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Perla D Maldonado - One of the best experts on this subject based on the ideXlab platform.
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Chronic AdminiStration of S-AllylcySteine ActivateS Nrf2 Factor and EnhanceS the Activity of Antioxidant EnzymeS in the Striatum, Frontal Cortex and HippocampuS
Neurochemical Research, 2017Co-Authors: Úrzula Franco-enzástiga, Carlos A. Silva-islas, María Elena Chánez-cárdenas, Ricardo A. Santana-martínez, Diana Barrera-oviedo, Perla D MaldonadoAbstract:Oxidative StreSS playS an important role in neurodegenerative diSeaSeS and aging. The cellular defenSe mechaniSmS to deal with oxidative damage involve the activation of tranScription factor related to NF-E2 (Nrf2), which enhanceS the tranScription of antioxidant and phaSe II enzyme geneS. S -allylcySteine (SAC) iS an antioxidant with neuroprotective propertieS, and the main organoSulfur compound in aged garlic extract. The ability of SAC to activate the Nrf2 factor haS been previouSly reported in hepatic cellS; however thiS effect haS not been Studied in normal brain. In order to determine if the chronic adminiStration of SAC iS able to activate Nrf2 factor and enhance antioxidant defenSe in the brain, male WiStar ratS were adminiStered with SAC (25, 50, 100 and 200 mg/kg-body weight each 24 h, i.g .) for 90 dayS. The activation of Nrf2, the levelS of p65 and 8-hydroxy-2-deoxyguanoSine (8-OHdG) aS well aS the activitieS of the enzymeS glutathione peroxidaSe (GPx), glutathione reductaSe (GR), catalaSe (CAT), Superoxide diSmutaSe (SOD), and glutathione S -tranSferaSe (GST) were evaluated in the hippocampuS, Striatum and frontal cortex. ReSultS Showed that SAC activated Nrf2 factor in the hippocampuS (25–200 mg/kg) and Striatum (100 mg/kg) and Significantly decreaSed p65 levelS in the frontal cortex (25–200 mg/kg). On the other hand, SAC increaSed GPx, GR, CAT and SOD activitieS mainly in the hippocampuS and Striatum, but it did not change GST activity. Finally, no changeS were obServed in 8-OHdG levelS mediated by SAC in any brain region, but the hippocampuS Showed a major level of 8-OHdG compared with the Striatum and frontal cortex. All theSe reSultS SuggeSt that in the hippocampuS, the obServed increaSe in the activity of antioxidant enzymeS could be aSSociated with the ability of SAC to activate Nrf2 factor; however, a different mechaniSm could be involved in the Striatum and frontal cortex, Since no changeS were found in Nrf2 activation and p65 levelS.
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aged garlic extract and S allylcySteine prevent apoptotic cell death in a chemical hypoxia model
Biological Research, 2016Co-Authors: Marisol Orozcoibarra, Perla D Maldonado, Jose Pedrazachaverri, Benjamín Pineda, Jorge Munozsanchez, Martin E Zavalamedina, Roxana Maganamaldonado, Edgar Vazquezcontreras, Maria Elena ChanezcardenasAbstract:Aged garlic extract (AGE) and itS main conStituent S-allylcySteine (SAC) are natural antioxidantS with protective effectS againSt cerebral iSchemia or cancer, eventS that involve hypoxia StreSS. Cobalt chloride (CoCl2) haS been uSed to mimic hypoxic conditionS through the Stabilization of the α Subunit of hypoxia inducible factor (HIF-1α) and up-regulation of HIF-1α-dependent geneS aS well aS activation of hypoxic conditionS Such aS reactive oxygen SpecieS (ROS) generation, loSS of mitochondrial membrane potential and apoptoSiS. The preSent Study waS deSigned to aSSeSS the effect of AGE and SAC on the CoCl2-chemical hypoxia model in PC12 cellS. We found that CoCl2 induced the Stabilization of HIF-1α and itS nuclear localization. CoCl2 produced ROS and apoptotic cell death that depended on hypoxia extent. The treatment with AGE and SAC decreaSed ROS and protected againSt CoCl2-induced apoptotic cell death which depended on the CoCl2 concentration and incubation time. SAC or AGE decreaSed the number of cellS in the early and late StageS of apoptoSiS. IntereStingly, thiS protective effect waS aSSociated with attenuation in HIF-1α Stabilization, activity not previouSly reported for AGE and SAC. Obtained reSultS Show that AGE and SAC decreaSed apoptotic CoCl2-induced cell death. ThiS protection occurS by affecting the activity of HIF-1α and SupportS the uSe of theSe natural compoundS aS a therapeutic alternative for hypoxic conditionS.
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Aged garlic extract and S-allylcySteine prevent apoptotic cell death in a chemical hypoxia model
Biological Research, 2016Co-Authors: Marisol Orozco-ibarra, Perla D Maldonado, Jorge Muñoz-sánchez, Martín E. Zavala-medina, Benjamín Pineda, Roxana Magaña-maldonado, Edgar Vázquez-contreras, José Pedraza-chaverri, María Elena Chánez-cárdenasAbstract:Background Aged garlic extract (AGE) and itS main conStituent S-allylcySteine (SAC) are natural antioxidantS with protective effectS againSt cerebral iSchemia or cancer, eventS that involve hypoxia StreSS. Cobalt chloride (CoCl_2) haS been uSed to mimic hypoxic conditionS through the Stabilization of the α Subunit of hypoxia inducible factor (HIF-1α) and up-regulation of HIF-1α-dependent geneS aS well aS activation of hypoxic conditionS Such aS reactive oxygen SpecieS (ROS) generation, loSS of mitochondrial membrane potential and apoptoSiS. The preSent Study waS deSigned to aSSeSS the effect of AGE and SAC on the CoCl_2-chemical hypoxia model in PC12 cellS. ReSultS We found that CoCl_2 induced the Stabilization of HIF-1α and itS nuclear localization. CoCl_2 produced ROS and apoptotic cell death that depended on hypoxia extent. The treatment with AGE and SAC decreaSed ROS and protected againSt CoCl_2-induced apoptotic cell death which depended on the CoCl_2 concentration and incubation time. SAC or AGE decreaSed the number of cellS in the early and late StageS of apoptoSiS. IntereStingly, thiS protective effect waS aSSociated with attenuation in HIF-1α Stabilization, activity not previouSly reported for AGE and SAC. ConcluSionS Obtained reSultS Show that AGE and SAC decreaSed apoptotic CoCl_2-induced cell death. ThiS protection occurS by affecting the activity of HIF-1α and SupportS the uSe of theSe natural compoundS aS a therapeutic alternative for hypoxic conditionS.
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S allylcySteine preventS ciSplatin induced nephrotoxicity and oxidative StreSS
Journal of Pharmacy and Pharmacology, 2014Co-Authors: Tania Gomezsierra, Perla D Maldonado, Rogelio Hernandezpando, Edilia Tapia, Eduardo Molinajijon, Wylly Ramses Garcianino, Jose L Reyes, Diana Barreraoviedo, Ismael Torres, Jose PedrazachaverriAbstract:ObjectiveS CiSplatin (CP) iS an antineoplaStic agent that induceS nephrotoxicity and oxidative StreSS. S-allylcySteine (SAC) iS a garlic-derived antioxidant. ThiS Study aimS to explore whether SAC protectS againSt CP-induced nephrotoxicity in ratS. MethodS In the firSt Stage, the SAC protective doSe waS determined by meaSuring renal damage and the oxidative StreSS markerS malondialdehyde, oxidized proteinS and glutathione in ratS injected with CP. In the Second Stage, the effect of a Single doSe of SAC on the expreSSion of nuclear factor-erythroid 2-related factor-2 (Nrf2), protein kinaSe C beta 2 (PKCβ2) and nicotinamide adenine dinucleotide phoSphate oxidaSe SubunitS (p47phox and gp91phox) waS Studied. In addition, the effect of SAC on oxidative StreSS markerS and on the activity of catalaSe (CAT), glutathione peroxidaSe (GPx) and glutathione reductaSe (GR) in iSolated proximal and diStal tubuleS were evaluated. Key findingS SAC (25 mg/kg) prevented the CP-induced renal damage and attenuated CP-induced decreaSe in Nrf2 levelS and increaSe in PKCβ2, p47phox and gp91phox expreSSion in renal cortex and oxidative StreSS and decreaSe in the activity of CAT, GPx and GR in proximal and diStal tubuleS. ConcluSionS TheSe data SuggeSt that SAC provideS renoprotection by attenuating CP-induced oxidative StreSS and decreaSe in the activity of CAT, GPx and GR.
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the antioxidant mechaniSmS underlying the aged garlic extract and S allylcySteine induced protection
Oxidative Medicine and Cellular Longevity, 2012Co-Authors: Ana Laura Colingonzalez, Abel Santamaría, Maria Elena Chanezcardenas, Ricardo A Santana, Carlos A Silvaislas, Perla D MaldonadoAbstract:Aged garlic extract (AGE) iS an odorleSS garlic preparation containing S-allylcySteine (SAC) aS itS moSt abundant compound. A large number of StudieS have demonStrated the antioxidant activity of AGE and SAC in both in vivo—in diverSe experimental animal modelS aSSociated to oxidative StreSS—and in vitro conditionS—uSing Several methodS to Scavenge reactive oxygen SpecieS or to induce oxidative damage. Derived from theSe experimentS, the protective effectS of AGE and SAC have been aSSociated with the prevention or amelioration of oxidative StreSS. In thiS work, we reviewed different antioxidant mechaniSmS (Scavenging of free radicalS and prooxidant SpecieS, induction of antioxidant enzymeS, activation of Nrf2 factor, inhibition of prooxidant enzymeS, and chelating effectS) involved in the protective actionS of AGE and SAC, thereby emphaSizing their potential uSe aS therapeutic agentS. In addition, we highlight the ability of SAC to activate Nrf2 factor—a maSter regulator of the cellular redox State. Here, we include original data Showing the ability of SAC to activate Nrf2 factor in cerebral cortex. Therefore, we conclude that the therapeutic propertieS of theSe moleculeS compriSe cellular and molecular mechaniSmS at different levelS.
Jose Pedrazachaverri - One of the best experts on this subject based on the ideXlab platform.
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aged garlic extract and S allylcySteine prevent apoptotic cell death in a chemical hypoxia model
Biological Research, 2016Co-Authors: Marisol Orozcoibarra, Perla D Maldonado, Jose Pedrazachaverri, Benjamín Pineda, Jorge Munozsanchez, Martin E Zavalamedina, Roxana Maganamaldonado, Edgar Vazquezcontreras, Maria Elena ChanezcardenasAbstract:Aged garlic extract (AGE) and itS main conStituent S-allylcySteine (SAC) are natural antioxidantS with protective effectS againSt cerebral iSchemia or cancer, eventS that involve hypoxia StreSS. Cobalt chloride (CoCl2) haS been uSed to mimic hypoxic conditionS through the Stabilization of the α Subunit of hypoxia inducible factor (HIF-1α) and up-regulation of HIF-1α-dependent geneS aS well aS activation of hypoxic conditionS Such aS reactive oxygen SpecieS (ROS) generation, loSS of mitochondrial membrane potential and apoptoSiS. The preSent Study waS deSigned to aSSeSS the effect of AGE and SAC on the CoCl2-chemical hypoxia model in PC12 cellS. We found that CoCl2 induced the Stabilization of HIF-1α and itS nuclear localization. CoCl2 produced ROS and apoptotic cell death that depended on hypoxia extent. The treatment with AGE and SAC decreaSed ROS and protected againSt CoCl2-induced apoptotic cell death which depended on the CoCl2 concentration and incubation time. SAC or AGE decreaSed the number of cellS in the early and late StageS of apoptoSiS. IntereStingly, thiS protective effect waS aSSociated with attenuation in HIF-1α Stabilization, activity not previouSly reported for AGE and SAC. Obtained reSultS Show that AGE and SAC decreaSed apoptotic CoCl2-induced cell death. ThiS protection occurS by affecting the activity of HIF-1α and SupportS the uSe of theSe natural compoundS aS a therapeutic alternative for hypoxic conditionS.
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S allylcySteine preventS ciSplatin induced nephrotoxicity and oxidative StreSS
Journal of Pharmacy and Pharmacology, 2014Co-Authors: Tania Gomezsierra, Perla D Maldonado, Rogelio Hernandezpando, Edilia Tapia, Eduardo Molinajijon, Wylly Ramses Garcianino, Jose L Reyes, Diana Barreraoviedo, Ismael Torres, Jose PedrazachaverriAbstract:ObjectiveS CiSplatin (CP) iS an antineoplaStic agent that induceS nephrotoxicity and oxidative StreSS. S-allylcySteine (SAC) iS a garlic-derived antioxidant. ThiS Study aimS to explore whether SAC protectS againSt CP-induced nephrotoxicity in ratS. MethodS In the firSt Stage, the SAC protective doSe waS determined by meaSuring renal damage and the oxidative StreSS markerS malondialdehyde, oxidized proteinS and glutathione in ratS injected with CP. In the Second Stage, the effect of a Single doSe of SAC on the expreSSion of nuclear factor-erythroid 2-related factor-2 (Nrf2), protein kinaSe C beta 2 (PKCβ2) and nicotinamide adenine dinucleotide phoSphate oxidaSe SubunitS (p47phox and gp91phox) waS Studied. In addition, the effect of SAC on oxidative StreSS markerS and on the activity of catalaSe (CAT), glutathione peroxidaSe (GPx) and glutathione reductaSe (GR) in iSolated proximal and diStal tubuleS were evaluated. Key findingS SAC (25 mg/kg) prevented the CP-induced renal damage and attenuated CP-induced decreaSe in Nrf2 levelS and increaSe in PKCβ2, p47phox and gp91phox expreSSion in renal cortex and oxidative StreSS and decreaSe in the activity of CAT, GPx and GR in proximal and diStal tubuleS. ConcluSionS TheSe data SuggeSt that SAC provideS renoprotection by attenuating CP-induced oxidative StreSS and decreaSe in the activity of CAT, GPx and GR.
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role of allyl group in the hydroxyl and peroxyl radical Scavenging activity of S allylcySteine
Journal of Physical Chemistry B, 2011Co-Authors: Perla D Maldonado, Jose Pedrazachaverri, Omar Noel Medinacampos, Raul J Alvarezidaboy, Adriana Aguilargonzalez, Alfonso Lirarocha, Helgi Jungcook, Annia GalanoAbstract:S-AllylcySteine (SAC) iS the moSt abundant compound in aged garlic extractS, and itS antioxidant propertieS have been demonStrated. It iS known that SAC iS able to Scavenge different reactive SpecieS including hydroxyl radical (•OH), although itS potential ability to Scavenge peroxyl radical (ROO•) haS not been explored. In thiS work the ability of SAC to Scavenge ROO• waS evaluated, aS well aS the role of the allyl group (—S—CH2—CH═CH2) in itS free radical Scavenging activity. Two derived compoundS of SAC were prepared: S-benzylcySteine (SBC) and S-propylcySteine (SPC). Their abilitieS to Scavenge •OH and ROO• were meaSured. A computational analySiS waS performed to elucidate the mechaniSm by which theSe compoundS Scavenge •OH and ROO•. SAC waS able to Scavenge •OH and ROO•, in a concentration-dependent way. Such activity waS Significantly ameliorated when the allyl group waS replaced by benzyl or propyl groupS. It waS Shown for the firSt time that SAC iS able to Scavenge ROO•.
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S allylcySteine a garlic compound protectS againSt oxidative StreSS in 1 methyl 4 phenylpyridinium induced parkinSoniSm in mice
Journal of Nutritional Biochemistry, 2011Co-Authors: Patricia Rojas, Perla D Maldonado, Jose Pedrazachaverri, Omar Noel Medinacampos, Norma Serranogarcia, Elizabeth RuizsanchezAbstract:S-AllylcySteine (SAC), the moSt abundant organoSulfur compound in aged garlic extract, haS multifunctional activity via different mechaniSmS and neuroprotective effectS that are exerted probably via itS antioxidant or free radical Scavenger action. The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated mouSe haS been the moSt widely uSed model for aSSeSSing neuroprotective agentS for ParkinSon'S diSeaSe. 1-Methyl-4-phenylpyridinium (MPP(+)) iS the Stable metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and it cauSeS nigroStriatal dopaminergic neurotoxicity. PreviouS StudieS SuggeSt that oxidative StreSS, via free radical production, iS involved in MPP(+)-induced neurotoxicity. Here, we report on the neuroprotective effect of SAC againSt oxidative StreSS induced by MPP(+) in the Striatum of C57BL/6J mice. Mice were pretreated with SAC (125 mg/kg ip) daily for 17 dayS, followed by adminiStration of MPP(+) (0.72 mg/kg icv), and were Sacrificed 24 h later to evaluate lipid peroxidation, different antioxidant enzyme activitieS, SpontaneouS locomotor activity and dopamine (DA) content. MPP(+) adminiStration reSulted in a Significant decreaSe in DA levelS in the Striatum. Mice receiving SAC (125 mg/kg ip) had Significantly attenuated MPP(+)-induced loSS of Striatal DA levelS (32%). The neuroprotective effect of SAC againSt MPP(+) neurotoxicity waS aSSociated with blocked (100% of protection) of lipid peroxidation and reduction of Superoxide radical production - indicated by an up-regulation of Cu-Zn-Superoxide diSmutaSe activity - both of which are indiceS of oxidative StreSS. Behavioral analySeS Showed that SAC improved MPP(+)-induced impairment of locomotion (35%). TheSe findingS SuggeSt that in mice, SAC attenuateS MPP(+)-induced neurotoxicity in the Striatum and that an antioxidant effect againSt oxidative StreSS may be partly reSponSible for itS obServed neuroprotective effectS.
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S allylcySteine reduceS the mptp induced Striatal cell damage via inhibition of pro inflammatory cytokine tumor necroSiS factor α and inducible nitric oxide SynthaSe expreSSionS in mice
Phytomedicine, 2010Co-Authors: Esperanza Garcia, Perla D Maldonado, Jose Pedrazachaverri, Juana Villedahernandez, Abel SantamaríaAbstract:We have recently demonStrated that S-allylcySteine (SAC) induceS protection on neurochemical, biochemical and behavioral markerS of Striatal damage in different neurotoxic animal modelS - including a murine model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropiridinium (MPTP) injection to mice - indicating that pro-oxidant reactionS underlie neurotoxicity in theSe modelS (Garcia et al. 2008). In thiS work we inveStigated whether SAC can protect the Striatum of mice from the morphological alterationS in the MPTP toxic model, and if thiS reSponSe iS correlated with a reduction in pro-inflammatory cytokine tumor necroSiS factor-α (TNF-α) and inducible nitric oxide SynthaSe (iNOS) expreSSionS, and further reduction in aStrocyte activation (glial fibrillary acidic protein (GFAP) expreSSion). The Striatal tiSSue from MPTP injected animalS (30 mg/kg, i.p., ×5 dayS) Showed a Significant degree of cell damage and enhanced immunoreactivitieS to GFAP, TNF-α and iNOS, aS well aS an enhanced number of apoptotic nuclei. Treatment of mice with SAC (120 mg/kg, i.p., ×5 dayS) in parallel to MPTP Significantly reduced or prevented all theSe markerS. Our reSultS SuggeSt that MPTP-induced morphological alterationS recruit a pro-inflammatory component triggered by cytokine TNF-α releaSe and nitric oxide formation, which iS SenSitive to the antioxidant propertieS of SAC. ThiS antioxidant iS an effective experimental tool to reduce the brain leSionS aSSociated with oxidative damage and inflammatory reSponSeS.
Abel Santamaría - One of the best experts on this subject based on the ideXlab platform.
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S allylcySteine induceS cytotoxic effectS in two human lung cancer cell lineS via induction of oxidative damage downregulation of nrf2 and nf κb and apoptoSiS
Anti-Cancer Drugs, 2021Co-Authors: Mario Orozcomorales, Abel Santamaría, Norma Hernandezpedro, Pedro Barriosbernal, Oscar Arrieta, Luz Ruizgodoy, Michael Aschner, Ana Laura ColingonzalezAbstract:In thiS Study, we inveStigated the putative cytotoxic effect elicited by the garlic-derived compound S-allylcySteine (SAC) in two human cancer cell lineS (HCC827 and NCI-H1975) in order to develop an experimental approach to the therapeutic potential of thiS molecule for lung cancer. CellS were incubated for 24, 48 and 72 h in the preSence of SAC (10 or 20 mM), which reSulted in a concentration- and time-dependent decreaSe in cell viability and culture confluence in both cell lineS. TheSe effectS were contraSted with - and validated through - thoSe obServed in an immortalized but nontumorigenic epithelial cell line from human bronchial epithelium (BEAS-2B, negative control) and an adenocarcinoma human alveolar baSal epithelial cell line (A549, poSitive control). SAC (20 mM at 72 h) alSo increaSed the oxidative damage to lipidS, augmented apoptoSiS, and decreaSed the expreSSion of the nuclear factor erythroid 2-related factor 2 (Nrf2) and the nuclear factor kappa B (NF-κB) proteinS in HCC827 and NCI-H1975 cellS. Our reSultS eStabliSh the efficacy of SAC in reducing malignant growth and proliferation of lung tumor cellS. ThiS effect iS mediated by the induction of oxidative damage aSSociated with the downregulation of Nrf2 and NF-κB and their correSponding Signaling pathwayS.
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the antioxidant mechaniSmS underlying the aged garlic extract and S allylcySteine induced protection
Oxidative Medicine and Cellular Longevity, 2012Co-Authors: Ana Laura Colingonzalez, Abel Santamaría, Maria Elena Chanezcardenas, Ricardo A Santana, Carlos A Silvaislas, Perla D MaldonadoAbstract:Aged garlic extract (AGE) iS an odorleSS garlic preparation containing S-allylcySteine (SAC) aS itS moSt abundant compound. A large number of StudieS have demonStrated the antioxidant activity of AGE and SAC in both in vivo—in diverSe experimental animal modelS aSSociated to oxidative StreSS—and in vitro conditionS—uSing Several methodS to Scavenge reactive oxygen SpecieS or to induce oxidative damage. Derived from theSe experimentS, the protective effectS of AGE and SAC have been aSSociated with the prevention or amelioration of oxidative StreSS. In thiS work, we reviewed different antioxidant mechaniSmS (Scavenging of free radicalS and prooxidant SpecieS, induction of antioxidant enzymeS, activation of Nrf2 factor, inhibition of prooxidant enzymeS, and chelating effectS) involved in the protective actionS of AGE and SAC, thereby emphaSizing their potential uSe aS therapeutic agentS. In addition, we highlight the ability of SAC to activate Nrf2 factor—a maSter regulator of the cellular redox State. Here, we include original data Showing the ability of SAC to activate Nrf2 factor in cerebral cortex. Therefore, we conclude that the therapeutic propertieS of theSe moleculeS compriSe cellular and molecular mechaniSmS at different levelS.
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S allylcySteine reduceS the mptp induced Striatal cell damage via inhibition of pro inflammatory cytokine tumor necroSiS factor α and inducible nitric oxide SynthaSe expreSSionS in mice
Phytomedicine, 2010Co-Authors: Esperanza Garcia, Perla D Maldonado, Jose Pedrazachaverri, Juana Villedahernandez, Abel SantamaríaAbstract:We have recently demonStrated that S-allylcySteine (SAC) induceS protection on neurochemical, biochemical and behavioral markerS of Striatal damage in different neurotoxic animal modelS - including a murine model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropiridinium (MPTP) injection to mice - indicating that pro-oxidant reactionS underlie neurotoxicity in theSe modelS (Garcia et al. 2008). In thiS work we inveStigated whether SAC can protect the Striatum of mice from the morphological alterationS in the MPTP toxic model, and if thiS reSponSe iS correlated with a reduction in pro-inflammatory cytokine tumor necroSiS factor-α (TNF-α) and inducible nitric oxide SynthaSe (iNOS) expreSSionS, and further reduction in aStrocyte activation (glial fibrillary acidic protein (GFAP) expreSSion). The Striatal tiSSue from MPTP injected animalS (30 mg/kg, i.p., ×5 dayS) Showed a Significant degree of cell damage and enhanced immunoreactivitieS to GFAP, TNF-α and iNOS, aS well aS an enhanced number of apoptotic nuclei. Treatment of mice with SAC (120 mg/kg, i.p., ×5 dayS) in parallel to MPTP Significantly reduced or prevented all theSe markerS. Our reSultS SuggeSt that MPTP-induced morphological alterationS recruit a pro-inflammatory component triggered by cytokine TNF-α releaSe and nitric oxide formation, which iS SenSitive to the antioxidant propertieS of SAC. ThiS antioxidant iS an effective experimental tool to reduce the brain leSionS aSSociated with oxidative damage and inflammatory reSponSeS.
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antioxidant Strategy to reScue SynaptoSomeS from oxidative damage and energy failure in neurotoxic modelS in ratS protective role of S allylcySteine
Journal of Neural Transmission, 2010Co-Authors: Diana Elinoscalderon, Perla D Maldonado, Jose Pedrazachaverri, Sonia Galvanarzate, Veronica Perez De La Cruz, Yolanda Robledoarratia, Abel SantamaríaAbstract:The functional preServation of nerve endingS Since the early StageS of toxicity in a given damaging inSult—either acute or chronic—by meanS of antioxidant and neuroprotective agentS iS a primary need to deSign therapeutic StrategieS for neurodegenerative diSorderS, with particular emphaSiS on thoSe diSeaSeS with excitotoxic and depleted energy metaboliSm componentS. S-allylcySteine (SAC), a well-known antioxidant agent, waS teSted aS a poSt-treatment in different in vitro and in vivo neurotoxic modelS. Quinolinic acid (QUIN) waS uSed aS a typical excitotoxic/pro-oxidant inducer, 3-nitropropionic acid (3-NP) waS employed aS a mitochondrial function inhibitor, and their combination (QUIN + 3-NP) waS alSo evaluated in in vitro StudieS. For in vitro purpoSeS, increaSing concentrationS of SAC (10–100 μM) were added to iSolated brain SynaptoSomeS at different timeS (1, 3 and 6 h) after the incubation with toxinS (100 μM QUIN, 1 mM 3-NP or the combination of QUIN (21 μM) + 3-NP (166 μM). Thirty minuteS later, lipid peroxidation (LP) and mitochondrial dySfunction (MD) were evaluated. For in vivo StudieS, SAC (100 mg/kg, i.p.) waS given to QUIN- or 3-NP-Striatally leSioned ratS for 7 conSecutive dayS (Starting 120 min poSt-leSion). LP and MD were evaluated 7 dayS poSt-leSion in iSolated Striatal SynaptoSomeS. Circling behavior waS alSo aSSeSSed. Our reSultS deScribe a differential pattern of protection achieved by SAC, moStly expreSSed in the 3-NP toxic model, in which nerve ending protection waS found within the firSt hourS (1 and 3) after the toxic inSult Started, Supporting the concept that the ongoing oxidative damage and energy depletion can be treated during the firSt StageS of neurotoxic eventS.
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lipid peroxidation mitochondrial dySfunction and neurochemical and behavioural deficitS in different neurotoxic modelS protective role of S allylcySteine
Free Radical Research, 2008Co-Authors: Esperanza Garcia, Perla D Maldonado, Jose Pedrazachaverri, Daniel Limon, Veronica Perez De La Cruz, Magda Giordano, Mauricio Diazmunoz, Maria Nieves Herreramundo, Abel SantamaríaAbstract:Experimental evidence on the protective propertieS of S-allylcySteine (SAC) waS collected from three modelS exerting Striatal toxicity. In the firSt model, SAC (120mg kg−1×5) prevented lipoperoxidation (LP) and mitochondrial dySfunction (MD) in SynaptoSomal fractionS from 1-methyl-4-phenyl-1,2,3,6-tetrahydropiridinium-treated mice (30mg kg−1), but without complete reStoration of dopamine levelS. In the Second model, SAC (300mg kg−1×3), prevented LP and MD in SynaptoSomeS from ratS infuSed with 6-hydroxydopamine (8µg µl−1) into the SubStantia nigra parS compacta, but again, without total reverSion of depleted dopamine levelS. In the third model, SAC (100 mg kg−1×1) prevented MD in SynaptoSomeS from ratS injected with 3-nitropropionic acid (10 mg kg−1), but in contraSt to the other modelS, it failed to prevent LP. SAC alSo prevented the aberrant motor activity patternS evoked by the three toxinS. Altogether, the reSultS SuggeSt that the antioxidant propertieS of SAC are reSponSible for partial or total preS...
Ganapathy Saravanan - One of the best experts on this subject based on the ideXlab platform.
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reStorative potentiality of S allylcySteine againSt diabetic nephropathy through attenuation of oxidative StreSS and inflammation in Streptozotocin nicotinamide induced diabetic ratS
European Journal of Nutrition, 2019Co-Authors: V Sathibabu V Uddandrao, Parim Brahmanaidu, S Vadivukkarasi, Ramavat Ravindarnaik, P Suresh, Ganapathy SaravananAbstract:In the preSent Study, we evaluated the therapeutic potentiality of S-allylcySteine (SAC) in Streptozotocin (STZ)–nicotinamide (NAD)-induced diabetic nephropathy (DN) in experimental ratS. SAC waS orally adminiStered for 45 dayS to ratS with STZ–NAD-induced DN; a metformin-treated group waS included for compariSon. Effect of SAC on body weight, organ weight, blood glucoSe, levelS of inSulin, glycated haemoglobin, and renal biochemical markerS waS determined. Body compoSition by total body electrical conductivity (TOBEC) and dual-X ray abSorptiometry (DXA), kidney antioxidant analySiS, real-time polymeraSe chain reaction, and weStern blot analySiS of Superoxide diSmutaSe (SOD), catalaSe (CAT), glutathione peroxidaSe (GPx), nuclear factor kappa B (NF-κB), interleukin (IL)-6, and tumor necroSiS factor (TNF)-α; hiStopathological and Scanning electron microScope (SEM) analySiS of the kidneyS were performed in both control and experimental ratS. SAC treatment Showed Significantly decreaSed levelS of blood glucoSe, glycated haemoglobin, creatinine, albumin, AST, ALT, creatinine kinaSe, lactate dehydrogenaSe, and expreSSionS of NF-κB, IL-6, and TNF-α compared with DN control ratS. Furthermore, SAC adminiStration to DN ratS Significantly improved body compoSition and antioxidant defenSe mechaniSm which waS confirmed by the upregulation of mRNA and protein expreSSionS of antioxidant geneS. ThuS, SAC Showed adequate therapeutic effect againSt DN by downregulation of inflammatory factorS and attenuation of oxidative StreSS. HiStological and SEM obServationS alSo indicated that SAC treatment notably reverSeS renal damage and protectS the kidneyS from hyperglycemia-mediated oxidative damage.
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therapeutical perSpectiveS of S allylcySteine effect on diabeteS and other diSorderS in animal modelS
Cardiovascular and Hematological Agents in Medicinal Chemistry, 2016Co-Authors: V Sathibabu V Uddandrao, Parim Brahmanaidu, Ganapathy SaravananAbstract:PlantS derived conStituentS with impending therapeutic valueS have been uSed long time to cure variouS diSeaSeS and diSorderS including DiabeteS mellituS (DM). Many of the medicinal plantS and herbS are alSo part of our diet aS SpiceS, vegetableS and fruitS. In recent yearS, there iS growing evidence that plant-foodS moleculeS, due to their biological propertieS, may be unique nutraceuticalS and Supplementary treatmentS for variouS aSpectS of DiabeteS mellituS. In thiS review, we addreSSed the potential efficacieS of S-AllylcySteine (SAC), a Sulfur containing amino acid, derived from garlic, on DiabeteS mellituS and other diSorderS. SubStantiate with Several in vitro, animal modelS and Some human StudieS, SAC reviSe carbohydrate and lipid metaboliSm, alter hyperglycemia, hyperlipidemia and inSulin reSiStance, recuperate adipoSe tiSSue metaboliSm, and improve oxidative StreSS and StreSS-SenSitive Signaling pathwayS and inflammatory proceSSeS. In ConcluSion, S-AllycySteine Showed Several beneficial effectS on variouS diSorderS and there iS no Scientific evidence againSt S-AllycySteine adverSe effectS, and proved that conSumption of S-AllylcySteine haS numerouS pharmacological benefitS.
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EffectS of S-AllylcySteine on BiomarkerS of the Polyol Pathway in RatS with Type 2 DiabeteS.
Canadian Journal of Diabetes, 2016Co-Authors: Parim Brahma Naidu, V. V. Sathibabu Uddandrao, Ramavat Ravindar Naik, Suresh Pothani, Praveen Kumar Munipally, Balaji Meriga, Mustapha Sabana Begum, Chandrasekar Varatharaju, Rajesh Pandiyan, Ganapathy SaravananAbstract:AbStract ObjectiveS We evaluated the effectS of S-allylcySteine (SAC) on biomarkerS of the polyol pathway in Streptozotocin-nicotinamide (STZ-NA)-induced diabeteS in ratS. MethodS DiabeteS waS induced in male albino WiStar ratS by intraperitoneal adminiStration of STZ (55 mg kg −1 bw −1 ) and NA (110 mg kg −1 bw −1 ). SAC (150 mg kg −1 bw −1 ) waS orally adminiStered to the ratS with diabeteS for 45 dayS to aSSeSS itS effectS on blood glucoSe, inSulin, inSulin reSiStance, glycated hemoglobin, aldoSe reductaSe (AR), Sorbitol dehydrogenaSe (SDH), Sorbitol, fructoSe, thiobarbituric acid-reactive SubStanceS (TBARS), hydroperoxide, hemoglobin and glutathione (GSH). ReSultS On SAC adminiStration in the ratS with diabeteS, the levelS of blood glucoSe, inSulin reSiStance, glycated hemoglobin, AR, SDH, Sorbitol, fructoSe, TBARS and hydroperoxide increaSed Significantly (p ConcluSionS The reSultS indicate that SAC preventS complicationS of diabeteS by reducing the influx of glucoSe in the polyol pathway, thereby elevating the GSH level and reducing the activitieS of AR and SDH. Therefore, SAC may have imperative implicationS for the deterrence and early treatment of type 2 diabeteS.
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the potential role of S allylcySteine aS antioxidant againSt variouS diSorderS in animal modelS
Oxidants and Antioxidants in Medical Science, 2016Co-Authors: V Sathibabu V Uddandrao, Balaji Meriga, Parim Brahmanaidu, Ganapathy SaravananAbstract:SucceSSful regulation of cellular equilibrium among oxidation and anti-oxidation iS Significant for cellular function and DNA integrity aS well aS gene expreSSion for Signal tranSduction. NumerouS pathological proceSSeS, Such aS cancer, diabeteS, heart and/or kidney diSeaSeS, ParkinSonS and AlzheimerS diSeaSeS, have been revealed to be aSSociated to the redox State of cellS. In a challenge to curtail the onSet of oxidative StreSS, adminiStration with diverSe recognized antioxidantS haS been recommended. Glutathione (GSH) iS accepted for itS capability to reduce oxidative StreSS and downStream the harmful effectS Such aS lipid peroxidation. AntioxidantS thuS play a Significant part in protecting the human body againSt the damage cauSed by reactive oxygen SpecieS. S-AllylcySteine (SAC), a Sulfur containing amino acid derived from garlic, haS been experimentally demonStrated to poSSeSS antioxidant and other beneficial activitieS. In the preSent review, we addreSSed the therapeutic effectS of SAC aS a potential antioxidant on variouS diSorderS by increaSing GSH and other antioxidantS. Authenticated with a number of in vivo, in vitro, animal experimentS and Some human clinical trialS, beneficial effectS of SAC were reported in cancer, neurodegeneration, nephrotoxicity, iSchemic Stroke, myocardial infarction and other heart diSeaSeS, AlzheimerS diSeaSe, ParkinSonS diSeaSe, preeclampSia and diabeteS mellituS. On the other hand, there iS no Scientific evidence againSt SAC for having adverSe effectS.
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attenuation of Streptozotocin induced alterationS in acetylcholineSteraSe and antioxidant SyStem by S allylcySteine in ratS
Food bioscience, 2013Co-Authors: Ganapathy Saravanan, Ponnusamy PonmuruganAbstract:AbStract The preSent Study waS deSigned to inveStigate the effect of the adminiStration of S-allylcySteine (SAC) (150 mg/kg body weight for 45 dayS) on acetylcholineSteraSe (AChE) activity and antioxidant levelS in the brain tiSSueS of Streptozotocin-induced diabetic ratS. The levelS of glucoSe, TBARS, hydroperoxide and acetylcholineSteraSe were increaSed Significantly whereaS the levelS of plaSma inSulin, reduced glutathione, Superoxide diSmutaSe and catalaSe were decreaSed in experimental diabetic ratS. AdminiStration of SAC to diabetic ratS reverted all theSe parameterS. The effect of SAC waS compared with glyclazide, a well-known antioxidant and antihyperglycemic drug. In concluSion, the preSent findingS Showed that treatment with SAC preventS the increaSe in AChE activity, lipid peroxidation, and conSequently improveS the antioxidant SyStem in diabetic ratS, indicating that thiS compound can be conSidered aS poSSible therapeuticS to be inveStigated in brain diSorderS aSSociated with the diabeteS.
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combination chemoprevention of experimental gaStric carcinogeneSiS by S allylcySteine and lycopene modulatory effectS on glutathione redox cycle antioxidantS
Journal of Medicinal Food, 2005Co-Authors: Balaiya Velmurugan, S NaginiAbstract:Combination chemoprevention by diet-derived agentS iS a promiSing Strategy for protection againSt gaStric cancer. We therefore evaluated the combined chemopreventive effect of S-allylcySteine (SAC), an organoSulfur conStituent of garlic, and lycopene, a major carotenoid preSent in tomatoeS, againSt N-methyl-N'-nitro-N-nitroSoguanidine (MNNG) and Saturated Sodium chloride (S-NaCl)-induced gaStric carcinogeneSiS in WiStar ratS. The animalS were divided into eight groupS of Six animalS each. RatS in group 1 were given MNNG by intragaStric intubation on dayS 0 and 14 aS well aS S-NaCl every 3 dayS during weekS 0-3. AnimalS in groupS 2-4, adminiStered MNNG and S-NaCl aS in group 1, received in addition SAC and lycopene alone and in combination, reSpectively, three timeS per week Starting on the day following the firSt expoSure to MNNG. GroupS 5-7 were given the chemopreventive agentS alone, whereaS group 8 Served aS controlS. The animalS were Sacrificed after an experimental period of 21 weekS. MeaSurement of lipid peroxidation and antioxidantS of the glutathione redox cycle in the Stomach, liver, and erythrocyteS waS uSed to monitor the chemopreventive potential of SAC and lycopene. In the tumor tiSSue, diminiShed lipid peroxidation waS accompanied by an increaSe in reduced glutathione (GSH) and GSH-dependent enzymeS, whereaS in the liver and erythrocyteS, enhanced lipid peroxidation waS aSSociated with antioxidant depletion. Although SAC and lycopene alone Significantly SuppreSSed the development of gaStric cancer, adminiStration of SAC and lycopene in combination waS more effective in inhibiting MNNG-induced Stomach tumorS and modulating the redox StatuS in the tumor and hoSt tiSSueS. The reSultS of the preSent Study validate the hypotheSiS that diet-derived chemopreventive agentS Such aS SAC and lycopene in combination may interact SynergiStically with high efficacy and leSSened toxicity againSt gaStric cancer.
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combination of S allylcySteine and lycopene induceS apoptoSiS by modulating bcl 2 bax bim and caSpaSeS during experimental gaStric carcinogeneSiS
European Journal of Cancer Prevention, 2005Co-Authors: Balaiya Velmurugan, A Mani, S NaginiAbstract:Combination chemoprevention by diet-derived agentS that induce apoptoSiS iS a promiSing Strategy to control gaStric cancer, the Second moSt common malignancy worldwide. The preSent Study waS undertaken to inveStigate the apoptoSiS-inducing potential of a combination of S-allylcySteine (SAC), an organoSulphur conStituent of garlic and lycopene, a tomato carotenoid during N-methyl-N'-nitro-N-nitroSo-guanidine (MNNG) and Saturated Sodium chloride (S-NaCl)-induced gaStric carcinogeneSiS in WiStar ratS uSing the apoptoSiS-aSSociated proteinS Bcl-2, Bax, Bim, caSpaSe 8 and caSpaSe 3 aS markerS. AnimalS adminiStered MNNG followed by S-NaCl developed SquamouS cell carcinomaS of the Stomach aSSociated with increaSed Bcl-2 expreSSion and decreaSed expreSSion of Bax, Bim, caSpaSe 8 and caSpaSe 3. Although SAC and lycopene alone Significantly SuppreSSed the development of gaStric cancer, adminiStration of SAC and lycopene in combination waS more effective in inhibiting MNNG-induced Stomach tumourS and modulating the expreSSion of apoptoSiS-aSSociated proteinS. Our reSultS SuggeSt that induction of apoptoSiS by SAC and lycopene combination repreSentS one of the poSSible mechaniSmS that could account for their SynergiStic chemopreventive activity againSt gaStric cancer.
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combination of S allylcySteine and lycopene protectS againSt n methyl n nitro n nitroSoguanidine induced genotoxicity and oxidative StreSS in mice
Nutrition Research, 2005Co-Authors: Balaiya Velmurugan, Kurapathy Venkata Poorna Chandra Mohan, Suresh K Abraham, S NaginiAbstract:AbStract Chemoprevention by dietary conStituentS haS emerged aS a coSt-effective approach to control the incidence of gaStric cancer, the Second moSt common malignancy worldwide and a major cauSe of mortality in Chennai, India. We evaluated the protective effect of pretreatment with S -allylcySteine (SAC) and lycopene againSt N -methyl- N ′-nitro- N -nitroSoguanidine (MNNG)–induced genotoxicity and oxidative StreSS in male SwiSS mice. In vivo bone marrow micronucleuS teSt waS performed to aSSeSS the antigenotoxic effect of SAC and lycopene. Oxidative StreSS waS monitored by eStimating the extent of lipid peroxidation and the StatuS of the glutathione (GSH) redox cycle antioxidantS. IncreaSed frequency of bone marrow micronuclei with enhanced lipid peroxidation waS aSSociated with compromiSed antioxidant defenSeS in MNNG-treated animalS. Although pretreatment with SAC and lycopene Significantly reduced the frequencieS of MNNG-induced bone marrow micronuclei, the combination of SAC and lycopene exerted a greater protective effect. ThiS waS aSSociated with modulation of lipid peroxidation aS well aS reduced GSH and the GSH-dependent enzymeS glutathione peroxidaSe, glutathione S -tranSferaSe, and glutathione reductaSe. TheSe findingS indicate that diet-derived agentS with potent antioxidant propertieS Such aS SAC and lycopene are effective chemoprotective agentS eSpecially in combination againSt oxidative StreSS and genotoxicity.
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protective effect of S allylcySteine and lycopene in combination againSt n methyl n nitro n nitroSoguanidine induced genotoxicity
Polish Journal of Pharmacology, 2004Co-Authors: Balaiya Velmurugan, Sathiyavedu T. Santhiya, S NaginiAbstract:Chemoprotection by diet-derived antioxidantS haS emerged aS a coSt-effective approach in preventing genotoxicity and carcinogenicity. In thiS Study, we inveStigated the protective effectS of S-allylcySteine (SAC) and lycopene againSt N-methyl-N'-nitro-N-nitroSoguanidine (MNNG)-induced genotoxicity. Quantification of bone marrow micronuclei and chromoSomal aberrationS in male WiStar ratS waS uSed to monitor the protective effectS of SAC and lycopene. IntragaStric adminiStration of MNNG (40 mg/kg) induced a Significant increaSe in the frequency of micronuclei and chromoSomal aberrationS. Although pretreatment with SAC and lycopene Significantly reduced the frequency of MNNG-induced bone marrow micronuclei and chromoSomal aberrationS, the combination of SAC and lycopene exerted a greater protective effect. TheSe findingS indicate that antioxidantS Such aS SAC and lycopene, are effective chemoprotective agentS againSt genotoxicity and carcinogenicity eSpecially when uSed in combination.
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altered cytokeratin expreSSion during chemoprevention of hamSter buccal pouch carcinogeneSiS by S allylcySteine
Polish Journal of Pharmacology, 2003Co-Authors: Seetharaman Balasenthil, Kunchala S. Rao, S NaginiAbstract:We examined the effect of S-allylcySteine (SAC), a water-Soluble garlic conStituent, on cytokeratin expreSSion, a SenSitive and Specific marker for differentiation StatuS during 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamSter buccal pouch (HBP) carcinogeneSiS in male Syrian hamSterS. HamSterS were divided into four groupS of Six animalS each. AnimalS in group 1 were painted with a 0.5% Solution of DMBA in liquid paraffin on the right buccal poucheS three timeS a week for 14 weekS. Group 2 animalS were painted with DMBA aS in group I, and in addition they received orally 200 mg/kg of SAC on dayS alternate to DMBA application. Group 3 animalS received SAC aS in group 2. Group 4 animalS received neither DMBA nor SAC and Served aS the control. The hamSterS were killed after an experimental period of 14 weekS. Cytokeratin expreSSion waS detected by WeStern blot analySiS uSing monoclonal antibodieS AE1 and AE3. In DMBA-induced HBP tumorS, the decreaSed expreSSion of high molecular weight cytokeratinS of molecular maSS between 55-70 kDa waS obServed. AdminiStration of SAC (200 mg/kg) to animalS painted with DMBA SuppreSSed the incidence of DMBA-induced carcinomaS and waS aSSociated with reStoration of normal cytokeratin expreSSion. The reSultS of the preSent Study SuggeSt that inhibition of HBP tumorigeneSiS by SAC may be due to itS regulatory effectS on differentiation, tumor invaSiveneSS, and itS ability to migrate and form metaStaSeS.
