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Wei Li - One of the best experts on this subject based on the ideXlab platform.

  • Maltol improves apap induced hepatotoxicity by inhibiting oxidative stress and inflammation response via nf κb and pi3k akt signal pathways
    Antioxidants, 2019
    Co-Authors: Zi Wang, Yingping Wang, Xiaojie Mi, Junnan Hu, Shuang Jiang, Xindian Li, Wei Li
    Abstract:

    Maltol, a food-flavoring agent and Maillard reaction product formed during the processing of red ginseng (Panax ginseng, C.A. Meyer), has been confirmed to exert a hepatoprotective effect in alcohol-induced oxidative damage in mice. However, its beneficial effects on acetaminophen (APAP)-induced hepatotoxicity and the related molecular mechanisms remain unclear. The purpose of this article was to investigate the protective effect and elucidate the mechanisms of action of Maltol on APAP-induced liver injury in vivo. Maltol was administered orally at 50 and 100 mg/kg daily for seven consecutive days, then a single intraperitoneal injection of APAP (250 mg/kg) was performed after the final Maltol administration. Liver function, oxidative indices, inflammatory factors—including serum alanine and aspartate aminotransferases (ALT and AST), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), liver glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), cytochrome P450 E1 (CYP2E1) and 4-hydroxynonenal (4-HNE) were measured. Results demonstrated that Maltol possessed a protective effect on APAP-induced liver injury. Liver histological changes and Hoechst 33258 staining also provided strong evidence for the protective effect of Maltol. Furthermore, a Maltol supplement mitigated APAP-induced inflammatory responses by increasing phosphorylated nuclear factor-kappa B (NF-κB), inhibitor kappa B kinase α/β (IKKα/β), and NF-kappa-B inhibitor alpha (IκBα) in NF-κB signal pathways. Immunoblotting results showed that Maltol pretreatment downregulated the protein expression levels of the B-cell-lymphoma-2 (Bcl-2) family and caspase and altered the phosphorylation of phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) in a dose-dependent manner. In conclusion, our findings clearly demonstrate that Maltol exerts a significant liver protection effect, which may partly be ascribed to its anti-inflammatory and anti-apoptotic action via regulation of the PI3K/Akt signaling pathway.

  • Maltol 3 hydroxy 2 methyl 4 pyrone slows d galactose induced brain aging process by damping the nrf2 ho 1 mediated oxidative stress in mice
    Journal of Agricultural and Food Chemistry, 2019
    Co-Authors: Yandan Zhou, Yingping Wang, Junnan Hu, Chen Chen, Jiayu Yang, Jing Leng, Jianhao Li, Shuang Jiang, Wei Li
    Abstract:

    Maltol, a maillard reaction product from ginseng (Panax ginseng C. A. Meyer), has been confirmed to inhibit oxidative stress in several animal models. Its beneficial effect on oxidative stress related brain aging is still unclear. In this study, the mouse model of d-galactose (d-Gal)-induced brain aging was employed to investigate the therapeutic effects and potential mechanisms of Maltol. Maltol treatment significantly restored memory impairment in mice as determined by the Morris water maze tests. Long-term d-Gal treatment reduced expression of cholinergic regulators, i.e., the cholineacetyltransferase (ChAT) (0.456 ± 0.10 vs 0.211 ± 0.03 U/mg prot), the acetylcholinesterase (AChE) (36.4 ± 5.21 vs 66.5 ± 9.96 U/g). Maltol treatment prevented the reduction of ChAT and AChE in the hippocampus. Maltol decreased oxidative stress levels by reducing levels of reactive oxygen species (ROS) and malondialdehyde (MDA) production in the brain and by elevating antioxidative enzymes. Furthermore, Maltol treatment mi...

  • Maltol mitigates thioacetamide induced liver fibrosis through tgf β1 mediated activation of pi3k akt signaling pathway
    Journal of Agricultural and Food Chemistry, 2019
    Co-Authors: Xiaojie Mi, Yingping Wang, Zi Wang, Chen Chen, Shuang Jiang, Shan Tang, Wei Li
    Abstract:

    Our previous study has confirmed that Maltol can attenuate alcohol-induced acute hepatic damage and prevent oxidative stress in mice. Therefore, Maltol might have the capacity to improve thioacetamide (TAA)-induced liver fibrosis. The purpose of this work was to explore the antifibrotic efficacy and underlying mechanisms of Maltol for TAA-treated mice. Progressive liver fibrosis was established with a dose-escalating protocol in which the mice received TAA intraperitoneal three times a week for a total duration of 9 weeks. The injection doses of TAA were 50 mg/kg for the first week, 100 mg/kg for the second and third weeks, and 150 mg/kg for the rest of the injections. Maltol with doses of 50 and 100 mg/kg was given by gavage after 4 weeks of intraperitoneal injection of TAA, respectively, once daily for 5 weeks. Results indicated that TAA intraperitoneal injection significantly increased serum activities of alanine aminotransferase (ALT) (52.93 ± 13.21 U/L vs 10.22 ± 3.36 U/L) and aspartate aminotransferase (AST) (67.58 ± 25.84 U/L vs 39.34 ± 3.89 U/L); these elevations were significantly diminished by pretreatment with Maltol. Additionally, Maltol ameliorated TAA-induced oxidative stress with attenuation in MDA (p < 0.05 or p < 0.01) content; evident elevation in the GSH levels, GSH/GSSG ratio (p < 0.05 or p < 0.01), and superoxide dismutase (SOD) (p < 0.01); and restored liver histology accompanied by a decrease of α-smooth muscle actin (α-SMA) expression. Furthermore, Maltol significantly suppressed the transforming growth factor-β1 (TGF-β1) expression and the PI3K/Akt pathway. This study suggested that Maltol alleviated experimental liver fibrosis by suppressing the activation of HSCs and inducing apoptosis of activated HSCs through TGF-β1-mediated PI3K/Akt signaling pathway. These findings further clearly suggested that Maltol is a potent therapeutic candidate for the alleviation of liver fibrosis.

  • the protective effects of Maltol on cisplatin induced nephrotoxicity through the ampk mediated pi3k akt and p53 signaling pathways
    Scientific Reports, 2018
    Co-Authors: Xiaojie Mi, Zi Wang, Junnan Hu, Chen Chen, Wei Li
    Abstract:

    Cisplatin, a potent anticancer drug, is usually causing nephrotoxicity; limiting its therapeutic application and efficiency. Maltol may be used to prevent such toxic effect. The aim of this study was to investigate the underlying protective mechanisms of Maltol on nephrotoxicity by cisplatin using a cisplatin-treated mouse model and a cellular toxicity model of HEK293 cells. The blood urea nitrogen (BUN), creatinine (CRE) and neutrophil gelatinase-associated lipocalin (NGAL) levels in mice were increased by cisplatin but decreased to normal ranges by Maltol pretreatment (50 and 100 mg/kg) for ten days. Besides, Maltol pretreatment decreased oxidative stress, lipid peroxidation and apoptosis in cisplatin-treated mice. The inhibitory action of Maltol on inflammatory responses was achieved by reducing the expressions in NF-κB, IL-1β, iNOS, and TNF-α in the mice in vivo. Additionally, Maltol restored the reduction of PI3K/Akt and mTOR levels by cisplatin through increasing AMPK expression in cisplatin-treated HEK293 cells. Maltol also suppressed the expression of Bax and caspase 3 by inhibiting the p53 activity in HEK293 cells. Overall, Maltol may serve as a valuable potential drug to prevent cisplatin-induced nephrotoxicity, and the underlying molecular mechanisms of Maltol action may involve intracellular AMPK/PI3K/Akt and p53 signaling pathways.

  • The protective effects of Maltol on cisplatin-induced nephrotoxicity through the AMPK-mediated PI3K/Akt and p53 signaling pathways.
    Scientific Reports, 2018
    Co-Authors: Xiaojie Mi, Zi Wang, Junnan Hu, Chen Chen, Wei Li
    Abstract:

    Cisplatin, a potent anticancer drug, is usually causing nephrotoxicity; limiting its therapeutic application and efficiency. Maltol may be used to prevent such toxic effect. The aim of this study was to investigate the underlying protective mechanisms of Maltol on nephrotoxicity by cisplatin using a cisplatin-treated mouse model and a cellular toxicity model of HEK293 cells. The blood urea nitrogen (BUN), creatinine (CRE) and neutrophil gelatinase-associated lipocalin (NGAL) levels in mice were increased by cisplatin but decreased to normal ranges by Maltol pretreatment (50 and 100 mg/kg) for ten days. Besides, Maltol pretreatment decreased oxidative stress, lipid peroxidation and apoptosis in cisplatin-treated mice. The inhibitory action of Maltol on inflammatory responses was achieved by reducing the expressions in NF-κB, IL-1β, iNOS, and TNF-α in the mice in vivo. Additionally, Maltol restored the reduction of PI3K/Akt and mTOR levels by cisplatin through increasing AMPK expression in cisplatin-treated HEK293 cells. Maltol also suppressed the expression of Bax and caspase 3 by inhibiting the p53 activity in HEK293 cells. Overall, Maltol may serve as a valuable potential drug to prevent cisplatin-induced nephrotoxicity, and the underlying molecular mechanisms of Maltol action may involve intracellular AMPK/PI3K/Akt and p53 signaling pathways.

Christopher K Thompson - One of the best experts on this subject based on the ideXlab platform.

  • the flavor enhancer Maltol increases pigment aggregation in dermal and neural melanophores in xenopus laevis tadpoles
    Environmental Toxicology and Chemistry, 2020
    Co-Authors: Lara Iza Dahora, Ashley Fitzgerald, Matthew Emanuel, Alexa Figueroa Baiges, Zahabiya Husain, Christopher K Thompson
    Abstract:

    Melanophores are pigmented cells that change the distribution of melanosomes, enabling animals to appear lighter or darker for camouflage, thermoregulation, and protection from ultraviolet radiation. A complex series of hormonal and neural mechanisms regulates melanophore pigment distribution, making these dynamic cells a valuable tool to screen toxicants as they rapidly respond to changes in the environment. We found that Maltol, a naturally occurring flavor enhancer and fragrance agent, induces melanophore pigment aggregation in a dose‐dependent manner in Xenopus laevis tadpoles. To determine if Maltol affects camouflage adaptation, we placed tadpoles into Maltol baths situated over either a white or a black background. Maltol induced pigment aggregation in a similar dose‐dependent pattern regardless of background color. We also tested how Maltol treatment compares to melatonin treatment and found that the degree of pigment aggregation induced by Maltol is similar to treatment with melatonin but that Maltol induces over a much longer time course. Last, Maltol had no effect on mRNA expression in the brain of genes that regulate camouflage‐related pigment aggregation. The present results suggest that Maltol does not exert its effects via the camouflage adaptation mechanism or via melatonin‐related mechanisms. These results are the first to identify a putative toxicological effect of Maltol exposure in vivo and rule out several mechanisms by which Maltol may exert its effects on pigment aggregation. Environ Toxicol Chem 2020;39:381–395. © 2019 SETAC

  • the flavor enhancer Maltol increases pigment aggregation in dermal and neural melanophores in xenopus laevis tadpoles
    bioRxiv, 2019
    Co-Authors: Lara Iza Dahora, Ashley Fitzgerald, Matthew Emanuel, Alexa Figueroa Baiges, Zahabiya Husain, Christopher K Thompson
    Abstract:

    Melanophores are pigmented cells that change the distribution of pigmented melanosomes, enabling animals to appear lighter or darker for camouflage, thermoregulation, and UV-protection. A complex series of hormonal and neural mechanisms regulates melanophore pigment distribution, making these cells a valuable tool to screen toxicants as a dynamic cell type that responds rapidly to the environment. We found that Maltol, a naturally occurring flavor enhancer and fragrance agent, induces melanophore pigment aggregation in a dose-dependent manner in Xenopus laevis tadpoles. To determine if Maltol affects camouflage adaptation, we placed tadpoles into Maltol baths situated over either white or black background. Maltol induced pigment aggregation in a similar dose-dependent pattern regardless of background color. We also tested how Maltol treatment compares to melatonin treatment and found that the degree of pigment aggregation induced by Maltol is similar to treatment with melatonin, but the time course differs significantly. Last, Maltol had no effect on mRNA expression of pro-opiomelanocortin or melanin concentrating hormone receptor in the brain, both of which regulate camouflage-related pigment aggregation. Our results suggest that Maltol does not exert its effects via the camouflage adaptation mechanism nor via melatonin-based mechanisms. These results are the first to identify a specific toxicological effect of Maltol exposure and rules out several mechanisms by which Maltol may exert its effects on pigment aggregation.

Yingping Wang - One of the best experts on this subject based on the ideXlab platform.

  • Maltol improves apap induced hepatotoxicity by inhibiting oxidative stress and inflammation response via nf κb and pi3k akt signal pathways
    Antioxidants, 2019
    Co-Authors: Zi Wang, Yingping Wang, Xiaojie Mi, Junnan Hu, Shuang Jiang, Xindian Li, Wei Li
    Abstract:

    Maltol, a food-flavoring agent and Maillard reaction product formed during the processing of red ginseng (Panax ginseng, C.A. Meyer), has been confirmed to exert a hepatoprotective effect in alcohol-induced oxidative damage in mice. However, its beneficial effects on acetaminophen (APAP)-induced hepatotoxicity and the related molecular mechanisms remain unclear. The purpose of this article was to investigate the protective effect and elucidate the mechanisms of action of Maltol on APAP-induced liver injury in vivo. Maltol was administered orally at 50 and 100 mg/kg daily for seven consecutive days, then a single intraperitoneal injection of APAP (250 mg/kg) was performed after the final Maltol administration. Liver function, oxidative indices, inflammatory factors—including serum alanine and aspartate aminotransferases (ALT and AST), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), liver glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), cytochrome P450 E1 (CYP2E1) and 4-hydroxynonenal (4-HNE) were measured. Results demonstrated that Maltol possessed a protective effect on APAP-induced liver injury. Liver histological changes and Hoechst 33258 staining also provided strong evidence for the protective effect of Maltol. Furthermore, a Maltol supplement mitigated APAP-induced inflammatory responses by increasing phosphorylated nuclear factor-kappa B (NF-κB), inhibitor kappa B kinase α/β (IKKα/β), and NF-kappa-B inhibitor alpha (IκBα) in NF-κB signal pathways. Immunoblotting results showed that Maltol pretreatment downregulated the protein expression levels of the B-cell-lymphoma-2 (Bcl-2) family and caspase and altered the phosphorylation of phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) in a dose-dependent manner. In conclusion, our findings clearly demonstrate that Maltol exerts a significant liver protection effect, which may partly be ascribed to its anti-inflammatory and anti-apoptotic action via regulation of the PI3K/Akt signaling pathway.

  • Maltol 3 hydroxy 2 methyl 4 pyrone slows d galactose induced brain aging process by damping the nrf2 ho 1 mediated oxidative stress in mice
    Journal of Agricultural and Food Chemistry, 2019
    Co-Authors: Yandan Zhou, Yingping Wang, Junnan Hu, Chen Chen, Jiayu Yang, Jing Leng, Jianhao Li, Shuang Jiang, Wei Li
    Abstract:

    Maltol, a maillard reaction product from ginseng (Panax ginseng C. A. Meyer), has been confirmed to inhibit oxidative stress in several animal models. Its beneficial effect on oxidative stress related brain aging is still unclear. In this study, the mouse model of d-galactose (d-Gal)-induced brain aging was employed to investigate the therapeutic effects and potential mechanisms of Maltol. Maltol treatment significantly restored memory impairment in mice as determined by the Morris water maze tests. Long-term d-Gal treatment reduced expression of cholinergic regulators, i.e., the cholineacetyltransferase (ChAT) (0.456 ± 0.10 vs 0.211 ± 0.03 U/mg prot), the acetylcholinesterase (AChE) (36.4 ± 5.21 vs 66.5 ± 9.96 U/g). Maltol treatment prevented the reduction of ChAT and AChE in the hippocampus. Maltol decreased oxidative stress levels by reducing levels of reactive oxygen species (ROS) and malondialdehyde (MDA) production in the brain and by elevating antioxidative enzymes. Furthermore, Maltol treatment mi...

  • Maltol mitigates thioacetamide induced liver fibrosis through tgf β1 mediated activation of pi3k akt signaling pathway
    Journal of Agricultural and Food Chemistry, 2019
    Co-Authors: Xiaojie Mi, Yingping Wang, Zi Wang, Chen Chen, Shuang Jiang, Shan Tang, Wei Li
    Abstract:

    Our previous study has confirmed that Maltol can attenuate alcohol-induced acute hepatic damage and prevent oxidative stress in mice. Therefore, Maltol might have the capacity to improve thioacetamide (TAA)-induced liver fibrosis. The purpose of this work was to explore the antifibrotic efficacy and underlying mechanisms of Maltol for TAA-treated mice. Progressive liver fibrosis was established with a dose-escalating protocol in which the mice received TAA intraperitoneal three times a week for a total duration of 9 weeks. The injection doses of TAA were 50 mg/kg for the first week, 100 mg/kg for the second and third weeks, and 150 mg/kg for the rest of the injections. Maltol with doses of 50 and 100 mg/kg was given by gavage after 4 weeks of intraperitoneal injection of TAA, respectively, once daily for 5 weeks. Results indicated that TAA intraperitoneal injection significantly increased serum activities of alanine aminotransferase (ALT) (52.93 ± 13.21 U/L vs 10.22 ± 3.36 U/L) and aspartate aminotransferase (AST) (67.58 ± 25.84 U/L vs 39.34 ± 3.89 U/L); these elevations were significantly diminished by pretreatment with Maltol. Additionally, Maltol ameliorated TAA-induced oxidative stress with attenuation in MDA (p < 0.05 or p < 0.01) content; evident elevation in the GSH levels, GSH/GSSG ratio (p < 0.05 or p < 0.01), and superoxide dismutase (SOD) (p < 0.01); and restored liver histology accompanied by a decrease of α-smooth muscle actin (α-SMA) expression. Furthermore, Maltol significantly suppressed the transforming growth factor-β1 (TGF-β1) expression and the PI3K/Akt pathway. This study suggested that Maltol alleviated experimental liver fibrosis by suppressing the activation of HSCs and inducing apoptosis of activated HSCs through TGF-β1-mediated PI3K/Akt signaling pathway. These findings further clearly suggested that Maltol is a potent therapeutic candidate for the alleviation of liver fibrosis.

  • the liver protection effects of Maltol a flavoring agent on carbon tetrachloride induced acute liver injury in mice via inhibiting apoptosis and inflammatory response
    Molecules, 2018
    Co-Authors: Zi Wang, Yingping Wang, Yandan Zhou, Shuang Jiang, Yufang He, Wei Li
    Abstract:

    The purpose of this research was to evaluate whether Maltol could protect from hepatic injury induced by carbon tetrachloride (CCl4) in vivo by inhibition of apoptosis and inflammatory responses. In this work, Maltol was administered at a level of 100 mg/kg for 15 days prior to exposure to a single injection of CCl4 (0.25%, i.p.). The results clearly indicated that the intrapulmonary injection of CCl4 resulted in a sharp increase in serum aspartate transaminase (AST) and alanine transaminase (ALT) activities, tumor necrosis factor-α (TNF-α), irreducible nitric oxide synthase (iNOS), nuclear factor-kappa B (NF-κB) and interleukin-1β (IL-1β) levels. Histopathological examination demonstrated severe hepatocyte necrosis and the destruction of architecture in liver lesions. Immunohistochemical staining and western blot analysis suggested an accumulation of iNOS, NF-κB, IL-1β and TNF-α expression. Maltol, when administered to mice for 15 days, can significantly improve these deleterious changes. In addition, TUNEL and Hoechst 33258 staining showed that a liver cell nucleus of a model group diffused uniform fluorescence following CCl4 injection. Maltol pretreatment groups did not show significant cell nuclear condensation and fragmentation, indicating that Maltol inhibited CCl4-induced cell apoptosis. By evaluating the liver catalase (CAT), glutathione (GSH), superoxide dismutase (SOD) activity, and further using a single agent to evaluate the oxidative stress in CCl4-induced hepatotoxicity by immunofluorescence staining, Maltol dramatically attenuated the reduction levels of hepatic CAT, GSH and SOD, and the over-expression levels of CYP2E1 and HO-1. In the mouse model of CCl4-induced liver injury, we have demonstrated that the inflammatory responses were inhibited, the serum levels of ALT and AST were reduced, cell apoptosis was suppressed, and liver injury caused by CCl4 was alleviated by Maltol, demonstrating that Maltol may be an efficient hepatoprotective agent.

  • Maltol a maillard reaction product exerts anti tumor efficacy in h22 tumor bearing mice via improving immune function and inducing apoptosis
    RSC Advances, 2015
    Co-Authors: Wei Li, Xiaomin Su, Qi Xu, Zi Wang, Jing Zhang, Yingping Wang
    Abstract:

    The purpose of this study was to investigate the anti-hepatoma activity of Maltol, a Maillard reaction product, in H22 tumor-bearing mice. The results demonstrate that Maltol not only significantly inhibited the growth of hepatoma H22 transplanted in mice, but also prolonged the survival time of H22-bearing mice. Furthermore, the levels of serum cytokines in H22 tumor-bearing mice, such as interferon gamma (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-2 (IL-2), were enhanced by Maltol treatment. Importantly, immunohistochemical and western blotting analysis clearly show that Maltol treatment increased Bax and decreased Bcl-2 protein expression levels of H22 tumor tissues in a dose-dependent manner. Collectively, our findings in the present study clearly demonstrate that the Maltol markedly suppressed the tumor growth of H22 transplanted tumors in vivo at least partly via improving the immune functions, inducing apoptosis, and inhibiting angiogenesis.

Lara Iza Dahora - One of the best experts on this subject based on the ideXlab platform.

  • the flavor enhancer Maltol increases pigment aggregation in dermal and neural melanophores in xenopus laevis tadpoles
    Environmental Toxicology and Chemistry, 2020
    Co-Authors: Lara Iza Dahora, Ashley Fitzgerald, Matthew Emanuel, Alexa Figueroa Baiges, Zahabiya Husain, Christopher K Thompson
    Abstract:

    Melanophores are pigmented cells that change the distribution of melanosomes, enabling animals to appear lighter or darker for camouflage, thermoregulation, and protection from ultraviolet radiation. A complex series of hormonal and neural mechanisms regulates melanophore pigment distribution, making these dynamic cells a valuable tool to screen toxicants as they rapidly respond to changes in the environment. We found that Maltol, a naturally occurring flavor enhancer and fragrance agent, induces melanophore pigment aggregation in a dose‐dependent manner in Xenopus laevis tadpoles. To determine if Maltol affects camouflage adaptation, we placed tadpoles into Maltol baths situated over either a white or a black background. Maltol induced pigment aggregation in a similar dose‐dependent pattern regardless of background color. We also tested how Maltol treatment compares to melatonin treatment and found that the degree of pigment aggregation induced by Maltol is similar to treatment with melatonin but that Maltol induces over a much longer time course. Last, Maltol had no effect on mRNA expression in the brain of genes that regulate camouflage‐related pigment aggregation. The present results suggest that Maltol does not exert its effects via the camouflage adaptation mechanism or via melatonin‐related mechanisms. These results are the first to identify a putative toxicological effect of Maltol exposure in vivo and rule out several mechanisms by which Maltol may exert its effects on pigment aggregation. Environ Toxicol Chem 2020;39:381–395. © 2019 SETAC

  • the flavor enhancer Maltol increases pigment aggregation in dermal and neural melanophores in xenopus laevis tadpoles
    bioRxiv, 2019
    Co-Authors: Lara Iza Dahora, Ashley Fitzgerald, Matthew Emanuel, Alexa Figueroa Baiges, Zahabiya Husain, Christopher K Thompson
    Abstract:

    Melanophores are pigmented cells that change the distribution of pigmented melanosomes, enabling animals to appear lighter or darker for camouflage, thermoregulation, and UV-protection. A complex series of hormonal and neural mechanisms regulates melanophore pigment distribution, making these cells a valuable tool to screen toxicants as a dynamic cell type that responds rapidly to the environment. We found that Maltol, a naturally occurring flavor enhancer and fragrance agent, induces melanophore pigment aggregation in a dose-dependent manner in Xenopus laevis tadpoles. To determine if Maltol affects camouflage adaptation, we placed tadpoles into Maltol baths situated over either white or black background. Maltol induced pigment aggregation in a similar dose-dependent pattern regardless of background color. We also tested how Maltol treatment compares to melatonin treatment and found that the degree of pigment aggregation induced by Maltol is similar to treatment with melatonin, but the time course differs significantly. Last, Maltol had no effect on mRNA expression of pro-opiomelanocortin or melanin concentrating hormone receptor in the brain, both of which regulate camouflage-related pigment aggregation. Our results suggest that Maltol does not exert its effects via the camouflage adaptation mechanism nor via melatonin-based mechanisms. These results are the first to identify a specific toxicological effect of Maltol exposure and rules out several mechanisms by which Maltol may exert its effects on pigment aggregation.

Hanxuan Ji - One of the best experts on this subject based on the ideXlab platform.

  • the investigation of the binding behavior between ethyl Maltol and human serum albumin by multi spectroscopic methods and molecular docking
    Spectrochimica Acta Part A: Molecular and Biomolecular Spectroscopy, 2012
    Co-Authors: Hanxuan Ji
    Abstract:

    Abstract This paper was designed to investigate the interaction of ethyl Maltol with human serum albumin (HSA) under physiological condition by fluorescence, synchronous fluorescence, three-dimensional fluorescence, Fourier transformation infrared spectra, and molecular docking method. Spectroscopic analysis of the emission quenching at different temperatures revealed that the quenching mechanism of HSA by ethyl Maltol was static quenching mechanism. The binding constants of ethyl Maltol–HSA complexes were observed to be 2.59, 1.88, 1.54, 1.13 × 10 4  M −1 at 289, 296, 303 and 310 K, respectively. The thermodynamic parameters, Δ H 0 and Δ S 0 were calculated to be −28.61 kJ mol −1 and −14.59 J mol −1  K −1 . Energy transfer from tryptophan to ethyl Maltol occurred by a FRET mechanism, and the donor–acceptor distance (3.04 nm) had been determined according to Forster’s theory. Molecular docking studies revealed that ethyl Maltol situated within subdomain IIA (site I) of HSA. Fluorescence displacement experiments also proved the binding sites between ethyl Maltol and HSA.