The Experts below are selected from a list of 2067 Experts worldwide ranked by ideXlab platform
Sudin Bhattacharya - One of the best experts on this subject based on the ideXlab platform.
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Amelioration of cisplatin-induced nephrotoxicity in mice by oral administration of diphenylmethyl Selenocyanate
Free radical research, 2010Co-Authors: Pramita Chakraborty, Somnath Singha Roy, Sudin BhattacharyaAbstract:AbstractCisplatin is one of the most potent and active cytotoxic drug in the treatment of cancer. However, side-effects in normal tissues and organs, notably nephrotoxicity in the kidneys, limit the promising efficacy of cisplatin. The present study was designed to ascertain the possible in vivo protective potential of a synthetic organoselenium compound diphenylmethyl Selenocyanate (3 mg/kg.b.w.) against the nephrotoxic damage induced by cisplatin (5 mg/kg.b.w. for 5 days) in Swiss albino mice. Treatment with diphenylmethyl Selenocyanate markedly reduced cisplatin-induced lipid peroxidation, serum creatinine and blood urea nitrogen levels. Renal antioxidant defense systems, such as glutathione-S-transferase, glutathione peroxidase, superoxide dismutase, catalase, activities and reduced glutathione level, depleted by cisplatin therapy, were restored to normal by the selenium compound. The selenium compound also reduced renal tubular epithelial cell damage, nitric oxide levels and expression of COX-2, and ...
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Modulation of Cyclophosphamide-Induced Cellular Toxicity by Diphenylmethyl Selenocyanate In Vivo, an Enzymatic Study
2009Co-Authors: Pramita Chakraborty, Ugir Hossain Sk, Nabendu Murmu, Sudin BhattacharyaAbstract:AIM: Cyclophosphamide (CP) is one of the most widely used alkylating antineoplastic agents that damage normal cells while killing cancerous cells in vivo. The use of CP in treating cancer patients is limited due to its severe toxicities induced mainly by oxidative stress. Diphenylmethyl Selenocyanate is a synthetic organoselenium compound shown to act as a potent antioxidant in chemically induced murine toxicity and carcinogenesis models in vivo. In the present study, this compound has been evaluated for its protective potential against CP-induced toxicity in Swiss albino mice. METHODS: CP was administered intraperitoneally (50 mg/kg) and diphenylmethyl Selenocyanate was given orally (3 mg/kg) in a pretreatment and concomitant treatment schedule, and the effects were assessed by estimating lipid peroxidation level, phase II detoxifying enzyme system, blood hemoglobin level, serum transaminase activity, and nitrite content. RESULTS: Diphenylmethyl Selenocyanate significantly (P＜0.05) increased glutathione-S-transferase, glutathione peroxidase, and catalase levels whereas decreased the lipid peroxidation levels in both liver and lung tissues of the animals given CP. Superoxide dismutase was increased significantly in liver (P＜0.05) but not in the lung. The selenium compound also significantly (P＜0.05) increased the blood hemoglobin level whereas decreased the transaminase activity in serum and the nitrite content in peritoneal macrophages. CONCLUSION: Our result suggests that diphenylmethyl Selenocyanate has the potential to prevent CP-induced cellular toxicity.
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Chemoprotection and enhancement of cancer chemotherapeutic efficacy of cyclophosphamide in mice bearing Ehrlich ascites carcinoma by diphenylmethyl Selenocyanate
Cancer Chemotherapy and Pharmacology, 2009Co-Authors: Pramita Chakraborty, Sudin BhattacharyaAbstract:Purpose Chemoprotective effect of diphenylmethyl Selenocyanate against cyclophosphamide (CP) induced cellular toxicity and antitumor efficacy was evaluated in mice bearing Ehrlich ascites carcinoma. Methods Diphenylmethyl Selenocyanate (3 mg/kg.b.w.) was administered orally and CP was given intraperitoneally (25 mg/kg.b.w). The effects were observed on the level of lipid peroxidation, antioxidant enzymes status, serum transaminase (ALT, AST) activity, hematological profile, transplantable murine tumor growth, apoptosis induction in tumor cells, and life span of tumor bearing hosts. Results The selenium compound restored the levels of antioxidant enzymes system, decreased the level of lipid peroxidation and serum transaminase activity. Hematological profile reverted to near normal level after selenium compound treatment. Treatment with the selenium compound also resulted in significant tumor growth regression along with significant upregulation of apoptosis, increased in mean survival time and life span of tumor bearing host. Conclusions Results clearly indicate that diphenylmethyl Selenocyanate has the potential to reduce the cellular toxicity of CP at the same time improving its antitumor efficacy.
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Chemoprotection and enhancement of cancer chemotherapeutic efficacy of cyclophosphamide in mice bearing Ehrlich ascites carcinoma by diphenylmethyl Selenocyanate.
Cancer chemotherapy and pharmacology, 2009Co-Authors: Pramita Chakraborty, Sudin BhattacharyaAbstract:Purpose Chemoprotective effect of diphenylmethyl Selenocyanate against cyclophosphamide (CP) induced cellular toxicity and antitumor efficacy was evaluated in mice bearing Ehrlich ascites carcinoma.
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Anti-tumour promoting activity of diphenylmethyl Selenocyanate against two-stage mouse skin carcinogenesis.
Asian Pacific journal of cancer prevention : APJCP, 2005Co-Authors: Rajat Kumar Das, Sudin BhattacharyaAbstract:Epidemiological, clinical and experimental evidence collectively suggests that Se in different inorganic and organic forms provides a potential cancer chemopreventive agent, active against several types of cancer. It can exert preventive activity in all the three stages of cancer: initiation, promotion and progression. Literature reports revealed that organoSelenocyanates have more potential as chemopreventive agents than inorganic forms due to their lower toxicity. In our previous report we showed chemopreventive efficacy of diphenylmethyl Selenocyanate during the initiation and pre- plus post-initiation phases of skin and colon carcinogenesis process. The present study was undertaken to explore the anti-tumour promoting activity of diphenylmethyl Selenocyanate in a 7,12-dimethylbenz (a) anthracene (DMBA)-croton oil two-stage skin carcinogenesis model. The results obtained showed significant (p
Pramita Chakraborty - One of the best experts on this subject based on the ideXlab platform.
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Amelioration of cisplatin-induced nephrotoxicity in mice by oral administration of diphenylmethyl Selenocyanate
Free radical research, 2010Co-Authors: Pramita Chakraborty, Somnath Singha Roy, Sudin BhattacharyaAbstract:AbstractCisplatin is one of the most potent and active cytotoxic drug in the treatment of cancer. However, side-effects in normal tissues and organs, notably nephrotoxicity in the kidneys, limit the promising efficacy of cisplatin. The present study was designed to ascertain the possible in vivo protective potential of a synthetic organoselenium compound diphenylmethyl Selenocyanate (3 mg/kg.b.w.) against the nephrotoxic damage induced by cisplatin (5 mg/kg.b.w. for 5 days) in Swiss albino mice. Treatment with diphenylmethyl Selenocyanate markedly reduced cisplatin-induced lipid peroxidation, serum creatinine and blood urea nitrogen levels. Renal antioxidant defense systems, such as glutathione-S-transferase, glutathione peroxidase, superoxide dismutase, catalase, activities and reduced glutathione level, depleted by cisplatin therapy, were restored to normal by the selenium compound. The selenium compound also reduced renal tubular epithelial cell damage, nitric oxide levels and expression of COX-2, and ...
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Modulation of Cyclophosphamide-Induced Cellular Toxicity by Diphenylmethyl Selenocyanate In Vivo, an Enzymatic Study
2009Co-Authors: Pramita Chakraborty, Ugir Hossain Sk, Nabendu Murmu, Sudin BhattacharyaAbstract:AIM: Cyclophosphamide (CP) is one of the most widely used alkylating antineoplastic agents that damage normal cells while killing cancerous cells in vivo. The use of CP in treating cancer patients is limited due to its severe toxicities induced mainly by oxidative stress. Diphenylmethyl Selenocyanate is a synthetic organoselenium compound shown to act as a potent antioxidant in chemically induced murine toxicity and carcinogenesis models in vivo. In the present study, this compound has been evaluated for its protective potential against CP-induced toxicity in Swiss albino mice. METHODS: CP was administered intraperitoneally (50 mg/kg) and diphenylmethyl Selenocyanate was given orally (3 mg/kg) in a pretreatment and concomitant treatment schedule, and the effects were assessed by estimating lipid peroxidation level, phase II detoxifying enzyme system, blood hemoglobin level, serum transaminase activity, and nitrite content. RESULTS: Diphenylmethyl Selenocyanate significantly (P＜0.05) increased glutathione-S-transferase, glutathione peroxidase, and catalase levels whereas decreased the lipid peroxidation levels in both liver and lung tissues of the animals given CP. Superoxide dismutase was increased significantly in liver (P＜0.05) but not in the lung. The selenium compound also significantly (P＜0.05) increased the blood hemoglobin level whereas decreased the transaminase activity in serum and the nitrite content in peritoneal macrophages. CONCLUSION: Our result suggests that diphenylmethyl Selenocyanate has the potential to prevent CP-induced cellular toxicity.
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Chemoprotection and enhancement of cancer chemotherapeutic efficacy of cyclophosphamide in mice bearing Ehrlich ascites carcinoma by diphenylmethyl Selenocyanate
Cancer Chemotherapy and Pharmacology, 2009Co-Authors: Pramita Chakraborty, Sudin BhattacharyaAbstract:Purpose Chemoprotective effect of diphenylmethyl Selenocyanate against cyclophosphamide (CP) induced cellular toxicity and antitumor efficacy was evaluated in mice bearing Ehrlich ascites carcinoma. Methods Diphenylmethyl Selenocyanate (3 mg/kg.b.w.) was administered orally and CP was given intraperitoneally (25 mg/kg.b.w). The effects were observed on the level of lipid peroxidation, antioxidant enzymes status, serum transaminase (ALT, AST) activity, hematological profile, transplantable murine tumor growth, apoptosis induction in tumor cells, and life span of tumor bearing hosts. Results The selenium compound restored the levels of antioxidant enzymes system, decreased the level of lipid peroxidation and serum transaminase activity. Hematological profile reverted to near normal level after selenium compound treatment. Treatment with the selenium compound also resulted in significant tumor growth regression along with significant upregulation of apoptosis, increased in mean survival time and life span of tumor bearing host. Conclusions Results clearly indicate that diphenylmethyl Selenocyanate has the potential to reduce the cellular toxicity of CP at the same time improving its antitumor efficacy.
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Chemoprotection and enhancement of cancer chemotherapeutic efficacy of cyclophosphamide in mice bearing Ehrlich ascites carcinoma by diphenylmethyl Selenocyanate.
Cancer chemotherapy and pharmacology, 2009Co-Authors: Pramita Chakraborty, Sudin BhattacharyaAbstract:Purpose Chemoprotective effect of diphenylmethyl Selenocyanate against cyclophosphamide (CP) induced cellular toxicity and antitumor efficacy was evaluated in mice bearing Ehrlich ascites carcinoma.
Marc Fourmigue - One of the best experts on this subject based on the ideXlab platform.
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Organic Selenocyanates as Halide Receptors: From Chelation to One-Dimensional Systems
Crystal Growth and Design, 2019Co-Authors: Asia Marie S. Riel, Olivier Jeannin, Huu-tri Huynh, Orion Berryman, Marc FourmigueAbstract:Organic Selenocyanates were recently identified as strong chalcogen bond donors. They also play an important role in biochemistry. Here, we show that 1,2-bis(selenocyanatomethyl)benzene (1) and 1,2,4,5-tetrakis(selenocyanatomethyl)-benzene (2) crystallize from dimethylformamide (DMF) to afford solvates where two ortho-SeCN moieties act as a chelate toward the carbonyl oxygen atom of DMF through strong Se···O chalcogen bonds. This result led us to explore their ability to also chelate halide anions (Cl–, Br–) in solution as well as in the solid state, an important issue in view of applications in crystal engineering or organocatalysis. NMR titration experiments provide an association constant between 1 and Cl– of 148 M–1. We also observed the recurrent formation of cocrystal salts from the association of the ChB donors 1 and 2 with the onium salts Ph4PCl, Ph4PBr, and Bu4NCl. We demonstrate that not only μ2-halide but also μ4-halide structures can be stabilized though ChB interactions, leading to the formation of complex polymeric anionic networks. Continuous shape measure calculations of these μ4-halide structures demonstrate that seesaw symmetry best describes the μ4-Br– bromide structures, while the smaller chloride anions tend to favor a close-to-tetrahedral μ4-Cl– organization, which is also confirmed by density functional theory calculations. Electrostatic surface potential calculations further demonstrate the efficiency of this chelating ortho-bis(selenocyanatomethyl) motif in 1 and 2, with Vs,max values reaching 50 kcal mol–1, to be compared with the simplest benzyl Selenocyanate (36.4 kcal mol–1) or the reference halogen bond donor F5C6–I (35.7 kcal mol–1) in the same conditions.
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Chalcogen bonding interactions in organic Selenocyanates From cooperativity to chelation
New Journal of Chemistry, 2018Co-Authors: O. Jeannin, H.-t. Huynh, A.m.s. Riel, Marc FourmigueAbstract:Intermolecular chalcogen bonding interactions are identified in crystalline organic Selenocyanates where a linear Se⋯NC interaction takes place, leading to the recurrent formation of chain-like motifs ⋯Se(R)-CN⋯Se(R)-CN⋯, stabilized by cooperativity. Analysis of 15 reported structures of such Selenocyanates is complemented by the structural determinations of three other novel polytopic Selenocyanates, namely 1,3,5-tris(selenocyanatomethyl)benzene (1a), 1,3,5-tris(selenocyanatomethyl)-2,4,6-trimethylbenzene (1b) and 1,2,4,5-tetrakis(selenocyanatomethyl)benzene (2). While the recurrent chain-like motifs with short and linear Se⋯N contacts are indeed observed in the pure compounds, solvates with DMF and AcOEt also demonstrate that the nitrile N atom can be easily displaced from the chalcogen bond by stronger Lewis bases such as carbonyl oxygen atoms, leading in the case of (2)·(DMF)2 to a chelating motif where two neighboring CH2-SeCN groups link to the same oxygen atom through Se⋯O interactions.
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Organic Selenocyanates as strong and directional chalcogen bond donors for crystal engineering.
Chemical Communications, 2017Co-Authors: Huu-tri Huynh, Olivier Jeannin, Marc FourmigueAbstract:Organic bis(Selenocyanate) derivatives act as powerful chalcogen bond donors for the elaboration of 1D extended structures upon co-crystallization with 4,4'-bipyridine as a ditopic chalcogen bond acceptor.
Brindaban C. Ranu - One of the best experts on this subject based on the ideXlab platform.
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Transition-Metal-Free Iodine Catalyzed Selenocayanation of Styrenyl Bromides and an Easy Access to Benzoselenophenes via Intermediacy of Styrenyl Selenocyanate
Organic letters, 2017Co-Authors: Pintu Maity, Bidisha Paroi, Brindaban C. RanuAbstract:A convenient procedure has been developed for the synthesis of styrenyl Selenocyanates and benzoselenophenes from readily available styrenyl bromides by reaction with potassium Selenocyanate in the presence of iodine under specified conditions. A series of both compounds have been obtained by this procedure. The synthesis of styrenyl Selenocyanates has not been previously reported, and thus this method is of much significance.
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Transition-Metal-Free Iodine Catalyzed Selenocayanation of Styrenyl Bromides and an Easy Access to Benzoselenophenes via Intermediacy of Styrenyl Selenocyanate
2017Co-Authors: Pintu Maity, Bidisha Paroi, Brindaban C. RanuAbstract:A convenient procedure has been developed for the synthesis of styrenyl Selenocyanates and benzoselenophenes from readily available styrenyl bromides by reaction with potassium Selenocyanate in the presence of iodine under specified conditions. A series of both compounds have been obtained by this procedure. The synthesis of styrenyl Selenocyanates has not been previously reported, and thus this method is of much significance
Carmen Sanmartín - One of the best experts on this subject based on the ideXlab platform.
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Organoseleno cytostatic derivatives: Autophagic cell death with AMPK and JNK activation.
European Journal of Medicinal Chemistry, 2019Co-Authors: Pablo Garnica, Ignacio Encío, Daniel Plano, Juan Antonio Palop, Carmen SanmartínAbstract:Abstract Selenocyanates and diselenides are potential antitumor agents. Here we report two series of selenium derivatives related to Selenocyanates and diselenides containing carboxylic, amide and imide moieties. These compounds were screened for their potency and selectivity against seven tumor cell lines and two non-malignant cell lines. Results showed that MCF-7 cells were especially sensitive to the treatment, with seven compounds presenting GI50 values below 10 μM. Notably, the carboxylic Selenocyanate 8b and the cyclic imide 10a also displayed high selectivity for tumor cells. Treatment of MCF-7 cells with these compounds resulted in cell cycle arrest at S phase, increased levels of pJNK and pAMPK and caspase independent cell death. Autophagy inhibitors wortmannin and chloroquine partially prevented 8b and 10a induced cell death. Consistent with autophagy, increased Beclin1 and LC3-IIB and reduced SQSTM1/p62 levels were detected. Our results point to 8b and 10a as autophagic cell death inducers.
