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Sidney J. Stohs - One of the best experts on this subject based on the ideXlab platform.

  • Endrin-induced depletion of glutathione and inhibition of glutathione peroxidase activity in rats.
    General Pharmacology-the Vascular System, 2003
    Co-Authors: I. T. Numan, M.q. Hassan, Sidney J. Stohs
    Abstract:

    1. Recent studies have shown that Endrin induces lipid peroxidation and may produce toxicity through an oxidative stress. We have therefore examined the effect of Endrin administration to rats on glutathione content and the activities of glutathione metabolizing enzymes. 2. The oral administration of Endrin resulted in dose- and time-dependent decreases in hepatic and renal glutathione content with maximum depletion (90%) occurring in liver at approximately 24 hr post-treatment. 3. Decreases in glutathione content were also observed in lung, brain, spleen and heart. 4. Endrin (4 mg/kg) decreased selenium dependent glutathione peroxidase activity in liver and kidney by 64 and 50%, respectively, while small increases were observed in the activities of glutathione reductase and glutathione S-transferase. 5. The toxicity of Endrin may be at least in part related to oxidative tissue damage associated with depletion of glutathione and inhibition of glutathione peroxidase activity.

  • comparative teratological studies on tcdd Endrin and lindane in c57bl 6j and dba 2j mice
    Comparative Biochemistry and Physiology Part C: Pharmacology Toxicology and Endocrinology, 1996
    Co-Authors: E. A. Hassoun, Sidney J. Stohs
    Abstract:

    Abstract The teratogenic effects of Endrin and lindane have been determined and compared to those induced by TCDD in the fetuses of C57BL/6J and DBA/2J mice after the administration of single oral doses to pregnant mice on day 12 of gestation. TCDD produced dose-dependent decreases in fetal weight, fetal thymic weight and placental weight, and dose-dependent increases in fetolethality, cleft palate formation and hydronephrosis at doses of 10–30 and 30–60 μg/kg body weight in C57BL/6J and DBA/2J mice, respectively. No maternal death was observed at the given doses in both strains of mice. Endrin (4.5 and 6 mg/kg body weight) and lindane (30 and 45 mg/kg body weight) produced significant decreases in fetal weight and placental weight in C57BL/6J and DBA/2J mice, and dose-dependent decreases in fetal thymic weight in C57BL/6J mice but not DBA/2J mice. Endrin and lindane caused 0–25 and 14–25% maternal deaths, respectively, at the above mentioned doses. Neither cleft plate nor hydronephrosis were induced by Endrin or lindane in the two strains of mice. The results support the hypothesis that TCDD-induced cleft plate and hydronephrosis involve mechanisms that are Ah (aryl hydrocarbon) receptor mediated. However, other fetotoxic effects induced by TCDD, and the fetotoxic effects induced by Endrin and lindane may involve additional unknown mechanisms that are not related to the Ah-receptor.

  • Comparative teratological studies on TCDD, Endrin and lindane in C57BL/6J and DBA/2J mice.
    Comparative biochemistry and physiology. Part C Pharmacology toxicology & endocrinology, 1996
    Co-Authors: E. A. Hassoun, Sidney J. Stohs
    Abstract:

    Abstract The teratogenic effects of Endrin and lindane have been determined and compared to those induced by TCDD in the fetuses of C57BL/6J and DBA/2J mice after the administration of single oral doses to pregnant mice on day 12 of gestation. TCDD produced dose-dependent decreases in fetal weight, fetal thymic weight and placental weight, and dose-dependent increases in fetolethality, cleft palate formation and hydronephrosis at doses of 10–30 and 30–60 μg/kg body weight in C57BL/6J and DBA/2J mice, respectively. No maternal death was observed at the given doses in both strains of mice. Endrin (4.5 and 6 mg/kg body weight) and lindane (30 and 45 mg/kg body weight) produced significant decreases in fetal weight and placental weight in C57BL/6J and DBA/2J mice, and dose-dependent decreases in fetal thymic weight in C57BL/6J mice but not DBA/2J mice. Endrin and lindane caused 0–25 and 14–25% maternal deaths, respectively, at the above mentioned doses. Neither cleft plate nor hydronephrosis were induced by Endrin or lindane in the two strains of mice. The results support the hypothesis that TCDD-induced cleft plate and hydronephrosis involve mechanisms that are Ah (aryl hydrocarbon) receptor mediated. However, other fetotoxic effects induced by TCDD, and the fetotoxic effects induced by Endrin and lindane may involve additional unknown mechanisms that are not related to the Ah-receptor.

  • comparative effects of Endrin on hepatic lipid peroxidation and dna damage and nitric oxide production by peritoneal macrophages from c57bl 6j and dba 2 mice
    Comparative Biochemistry and Physiology Part C: Comparative Pharmacology, 1993
    Co-Authors: Manashi Bagchi, E. A. Hassoun, Debasis Bagchi, P L Akubue, Sidney J. Stohs
    Abstract:

    Abstract 1. Endrin is a polyhalogenated cyclic hydrocarbon which produces hepatic and neurologic toxicity. In order to further assess the mechanism of toxicity ofEndrin, the dose-dependent effects of Endrin on hepatic lipid peroxidation and DNA damage, and nitric oxide (NO) production by peritoneal exudate cells (primarily macrophages) were investigated in C57BL/6J and DBA/2 mice which vary at the Ah receptor genetic locus. C57BL/6J mice are dioxin-responsive, while DBA/2 mice are dioxin-insensitive. 2. Mice of both strains were treated with 0, 1, 2 or 4 mg Endrin kg −1 as a single oral dose in corn oil, and the animals were killed 24 hr post-treatment. At doses of 1,2 and 4 mg Endrin kg −1 in C57BL/6J mice, hepatic mitochondrial lipid peroxidation increased 1.2-, 2.2- and 3.2-fold, respectively, and 1.8-, 2.3- and 3.5-fold with microsomes, respectively. At these same doses in DBA/2 mice, hepatic mitochondrial lipid peroxidation increased 1.3-, 2.0- and 2.6-fold, respectively, and 1.5-, 1.9- and 2.5-fold with microsomes, respectively. 3. Increases of 2.3-, 2.4- and 4.9-fold were observed in hepatic DNA damage (elution constants) in C57BL/6J mice at doses of 1, 2 and 4 mg Endrin kg −1 , respectively, while at these same three doses, increases of 1.9-, 2.1- and 2.3-fold were observed for DBA/2 mice, respectively. 4. Nitric oxide production by peritoneal macrophages from C57BL/6J increased by 1.3-, 1.7- and 2.0-fold with doses of 1, 2 and 4 mg Endrin kg −1 , respectively, while in macrophages from DBA/2 mice at these same doses, increases of 1.7-, 1.7- and 1.8-fold, respectively, were observed. 5. The results indicate that the responsiveness of peritoneal macrophages with respect to both DNA damage and nitric oxide production are more dose-dependent in C57BL/6J mice as compared to DBA/2 mice, while similar results are observed with the lipid peroxidation of hepatic mitochondria and microsomes of the two mouse strains. The results suggest that the toxicity of Endrin is less reliant on a mechanism which may involve the Ah receptor system as compared to dioxins as 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD).

  • production of reactive oxygen species by peritoneal macrophages and hepatic mitochondria and microsomes from Endrin treated rats
    Free Radical Biology and Medicine, 1993
    Co-Authors: Manashi Bagchi, E. A. Hassoun, Debasis Bagchi, Sidney J. Stohs
    Abstract:

    Abstract Recent studies have shown that the adminstration of endrn to rodents induced lipid peroxidation in various tissues and decreases glutathione content. These results suggest that Endrin produces reactive oxygen species and/or free radicals. We have therefore examined the effects of Endrin(4.5 mg/kg) on the production of reactive oxygen species by peritoneal macrophages and hepatic mitochondria and microsomes in rats. The effects of Endrin on hepatic mitochondrial and microsomal lipid peroxidation and membrane fluidity as well as the incidence of hepatic nuclear DNA damage were also examined. Twenty-four hours after Endrin administration, significant increases in the production of the chemiluminescence by the three tissue fractions were observed. Furthermore, peritoneal macrophages form Endrin-animals resulted in 3.0- and 2.8-fold increases in cytochrome c and iodonitrotetrazolium (INT) reduction, indicating enhanced production of superoxide anion. Endrin administration also resulted in significant increases in lipid peroxidation of mitochondrial and microsomal membranes as well as decreases in the fluidity of these two membranous fractions. A significant increase in hepatic nuclear DNA single-strand breaks also occurred in response to Endrin administration. The reslts indicate that macrophage, mitochondria, and microsomes produce reactive oxygen species following Endrin administration, and these reactive oxygen species may contribute to the toxic manifestations of Endrin.

E. A. Hassoun - One of the best experts on this subject based on the ideXlab platform.

  • comparative teratological studies on tcdd Endrin and lindane in c57bl 6j and dba 2j mice
    Comparative Biochemistry and Physiology Part C: Pharmacology Toxicology and Endocrinology, 1996
    Co-Authors: E. A. Hassoun, Sidney J. Stohs
    Abstract:

    Abstract The teratogenic effects of Endrin and lindane have been determined and compared to those induced by TCDD in the fetuses of C57BL/6J and DBA/2J mice after the administration of single oral doses to pregnant mice on day 12 of gestation. TCDD produced dose-dependent decreases in fetal weight, fetal thymic weight and placental weight, and dose-dependent increases in fetolethality, cleft palate formation and hydronephrosis at doses of 10–30 and 30–60 μg/kg body weight in C57BL/6J and DBA/2J mice, respectively. No maternal death was observed at the given doses in both strains of mice. Endrin (4.5 and 6 mg/kg body weight) and lindane (30 and 45 mg/kg body weight) produced significant decreases in fetal weight and placental weight in C57BL/6J and DBA/2J mice, and dose-dependent decreases in fetal thymic weight in C57BL/6J mice but not DBA/2J mice. Endrin and lindane caused 0–25 and 14–25% maternal deaths, respectively, at the above mentioned doses. Neither cleft plate nor hydronephrosis were induced by Endrin or lindane in the two strains of mice. The results support the hypothesis that TCDD-induced cleft plate and hydronephrosis involve mechanisms that are Ah (aryl hydrocarbon) receptor mediated. However, other fetotoxic effects induced by TCDD, and the fetotoxic effects induced by Endrin and lindane may involve additional unknown mechanisms that are not related to the Ah-receptor.

  • Comparative teratological studies on TCDD, Endrin and lindane in C57BL/6J and DBA/2J mice.
    Comparative biochemistry and physiology. Part C Pharmacology toxicology & endocrinology, 1996
    Co-Authors: E. A. Hassoun, Sidney J. Stohs
    Abstract:

    Abstract The teratogenic effects of Endrin and lindane have been determined and compared to those induced by TCDD in the fetuses of C57BL/6J and DBA/2J mice after the administration of single oral doses to pregnant mice on day 12 of gestation. TCDD produced dose-dependent decreases in fetal weight, fetal thymic weight and placental weight, and dose-dependent increases in fetolethality, cleft palate formation and hydronephrosis at doses of 10–30 and 30–60 μg/kg body weight in C57BL/6J and DBA/2J mice, respectively. No maternal death was observed at the given doses in both strains of mice. Endrin (4.5 and 6 mg/kg body weight) and lindane (30 and 45 mg/kg body weight) produced significant decreases in fetal weight and placental weight in C57BL/6J and DBA/2J mice, and dose-dependent decreases in fetal thymic weight in C57BL/6J mice but not DBA/2J mice. Endrin and lindane caused 0–25 and 14–25% maternal deaths, respectively, at the above mentioned doses. Neither cleft plate nor hydronephrosis were induced by Endrin or lindane in the two strains of mice. The results support the hypothesis that TCDD-induced cleft plate and hydronephrosis involve mechanisms that are Ah (aryl hydrocarbon) receptor mediated. However, other fetotoxic effects induced by TCDD, and the fetotoxic effects induced by Endrin and lindane may involve additional unknown mechanisms that are not related to the Ah-receptor.

  • protective effects of lazaroid u74389f 16 desmethyl tirilazad on Endrin induced lipid peroxidation and dna damage in brain and liver and regional distribution of catalase activity in rat brain
    Free Radical Biology and Medicine, 1995
    Co-Authors: M. Bagchi, E. A. Hassoun, D. Bagchi, S Ghosh, S. J. Stohs
    Abstract:

    Abstract Endrin, a poly-halogenated cyclic hydrocarbon, induces hepatic lipid peroxidation, modulates calcium homeostasis, decreases membrane fluidity, and increases nuclear DNA damage. Little information is available on the neurotoxicity of Endrin. The effects of Endrin on lipid peroxidation, DNA damage, and regional distribution of catalase activity were assessed in rat brain and liver 24 h following an acute oral dose of 4.5 mg Endrin/kg. Lipid peroxidation associated with whole brain mitochondria increased 2.4-fold, whereas microsomal lipid peroxidation increased 2.8-fold following Endrin administration. Lipid peroxidation also increased 2.0-fold both in hepatic mitochondria and microsomes. Catalase activity decreased 24% in the hypothalamus, 23% in the cortex, 38% in the cerebellum, and 11% in the brain stem in response to Endrin. A 4.3-fold increase in brain nuclear DNA-single strand breaks (SSB) was observed in Endrin-treated rats. Pretreatment of rats intraperitoneally with the lazaroid U74389F (16-desmethyl tirilazad) (10 mg/kg in two doses) attenuated the biochemical consequences of Endrin-induced oxidative stress. The administration of U74389F in citrate buffer (pH 3.8) provided better protection than administering the lazaroid in corn oil, decreasing Endrin-induced lipid peroxidation by 50–80% and DNA-SSB by approximately 72% in liver and 85% in brain, while ameliorating the suppressed catalase activity. The data suggest an involvement of an oxidative stress in the neurotoxicity and hepatotoxicity induced by Endrin, which can be attenuated by the lazaroid U74389F.

  • comparative effects of Endrin on hepatic lipid peroxidation and dna damage and nitric oxide production by peritoneal macrophages from c57bl 6j and dba 2 mice
    Comparative Biochemistry and Physiology Part C: Comparative Pharmacology, 1993
    Co-Authors: Manashi Bagchi, E. A. Hassoun, Debasis Bagchi, P L Akubue, Sidney J. Stohs
    Abstract:

    Abstract 1. Endrin is a polyhalogenated cyclic hydrocarbon which produces hepatic and neurologic toxicity. In order to further assess the mechanism of toxicity ofEndrin, the dose-dependent effects of Endrin on hepatic lipid peroxidation and DNA damage, and nitric oxide (NO) production by peritoneal exudate cells (primarily macrophages) were investigated in C57BL/6J and DBA/2 mice which vary at the Ah receptor genetic locus. C57BL/6J mice are dioxin-responsive, while DBA/2 mice are dioxin-insensitive. 2. Mice of both strains were treated with 0, 1, 2 or 4 mg Endrin kg −1 as a single oral dose in corn oil, and the animals were killed 24 hr post-treatment. At doses of 1,2 and 4 mg Endrin kg −1 in C57BL/6J mice, hepatic mitochondrial lipid peroxidation increased 1.2-, 2.2- and 3.2-fold, respectively, and 1.8-, 2.3- and 3.5-fold with microsomes, respectively. At these same doses in DBA/2 mice, hepatic mitochondrial lipid peroxidation increased 1.3-, 2.0- and 2.6-fold, respectively, and 1.5-, 1.9- and 2.5-fold with microsomes, respectively. 3. Increases of 2.3-, 2.4- and 4.9-fold were observed in hepatic DNA damage (elution constants) in C57BL/6J mice at doses of 1, 2 and 4 mg Endrin kg −1 , respectively, while at these same three doses, increases of 1.9-, 2.1- and 2.3-fold were observed for DBA/2 mice, respectively. 4. Nitric oxide production by peritoneal macrophages from C57BL/6J increased by 1.3-, 1.7- and 2.0-fold with doses of 1, 2 and 4 mg Endrin kg −1 , respectively, while in macrophages from DBA/2 mice at these same doses, increases of 1.7-, 1.7- and 1.8-fold, respectively, were observed. 5. The results indicate that the responsiveness of peritoneal macrophages with respect to both DNA damage and nitric oxide production are more dose-dependent in C57BL/6J mice as compared to DBA/2 mice, while similar results are observed with the lipid peroxidation of hepatic mitochondria and microsomes of the two mouse strains. The results suggest that the toxicity of Endrin is less reliant on a mechanism which may involve the Ah receptor system as compared to dioxins as 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD).

  • production of reactive oxygen species by peritoneal macrophages and hepatic mitochondria and microsomes from Endrin treated rats
    Free Radical Biology and Medicine, 1993
    Co-Authors: Manashi Bagchi, E. A. Hassoun, Debasis Bagchi, Sidney J. Stohs
    Abstract:

    Abstract Recent studies have shown that the adminstration of endrn to rodents induced lipid peroxidation in various tissues and decreases glutathione content. These results suggest that Endrin produces reactive oxygen species and/or free radicals. We have therefore examined the effects of Endrin(4.5 mg/kg) on the production of reactive oxygen species by peritoneal macrophages and hepatic mitochondria and microsomes in rats. The effects of Endrin on hepatic mitochondrial and microsomal lipid peroxidation and membrane fluidity as well as the incidence of hepatic nuclear DNA damage were also examined. Twenty-four hours after Endrin administration, significant increases in the production of the chemiluminescence by the three tissue fractions were observed. Furthermore, peritoneal macrophages form Endrin-animals resulted in 3.0- and 2.8-fold increases in cytochrome c and iodonitrotetrazolium (INT) reduction, indicating enhanced production of superoxide anion. Endrin administration also resulted in significant increases in lipid peroxidation of mitochondrial and microsomal membranes as well as decreases in the fluidity of these two membranous fractions. A significant increase in hepatic nuclear DNA single-strand breaks also occurred in response to Endrin administration. The reslts indicate that macrophage, mitochondria, and microsomes produce reactive oxygen species following Endrin administration, and these reactive oxygen species may contribute to the toxic manifestations of Endrin.

Hiroshi Oyaizu - One of the best experts on this subject based on the ideXlab platform.

  • Bioremediation of the organochlorine pesticides, dieldrin and Endrin, and their occurrence in the environment
    Applied Microbiology and Biotechnology, 2009
    Co-Authors: Emiko Matsumoto, Youhei Kawanaka, Sun-ja Yun, Hiroshi Oyaizu
    Abstract:

    Dieldrin and Endrin are persistent organic pollutants that cause serious environmental problems. Although these compounds have been prohibited over the past decades in most countries around the world, they are still routinely found in the environment, especially in the soil in agricultural fields. Bioremediation, including phytoremediation and rhizoremediation, is expected to be a useful cleanup method for this soil contamination. This review provides an overview of the environmental contamination by dieldrin and Endrin, along with a summary of our current understanding and recent advances in bioremediation and phytoremediation of these pollutants. In particular, this review focuses on the types and abilities of plants and microorganisms available for accumulating and degrading dieldrin and Endrin.

  • Isolation of dieldrin- and Endrin-degrading bacteria using 1,2-epoxycyclohexane as a structural analog of both compounds.
    Applied microbiology and biotechnology, 2008
    Co-Authors: Emiko Matsumoto, Youhei Kawanaka, Sun-ja Yun, Hiroshi Oyaizu
    Abstract:

    This report describes the selective isolation of dieldrin- and Endrin-degrading bacteria from soil with high degradation activity toward dieldrin and Endrin. Several enrichment cultures from the soil were arranged with several structural analogs of dieldrin and Endrin as a growth substrate and examined for their degradation activities toward dieldrin and Endrin. An enrichment culture with 1,2-epoxycyclohexane (ECH) was found to aerobically degrade dieldrin and Endrin. Denaturing gradient gel electrophoresis (DGGE) indicated that three types of bacteria were predominant in the ECH enrichment culture. Of the three major bacteria, two isolates, Burkholderia sp. strain MED-7 and Cupriavidus sp. strain MED-5, showed high degradation activity toward dieldrin and Endrin. The degradation efficiencies of strain MED-7 and MED-5 were 49% and 38% toward dieldrin, respectively, and 51% and 40% toward Endrin, respectively, in the presence of ECH for 14 days. These results indicated that ECH was a useful substrate for selective and efficient isolation of dieldrin- and Endrin-degrading bacteria from soil containing numerous bacteria. Interestingly, the two isolates could also degrade dieldrin and Endrin even in the absence of ECH. These are the first microorganisms demonstrated to grow on dieldrin and Endrin as the sole carbon and energy source under aerobic conditions.

Zhaokun Luan - One of the best experts on this subject based on the ideXlab platform.

  • Sorption of Endrin to montmorillonite and kaolinite clays.
    Journal of hazardous materials, 2009
    Co-Authors: Xianjia Peng, Jun Wang, Bin Fan, Zhaokun Luan
    Abstract:

    It has been discovered previously that clay minerals may have a greater potential for sorption of pesticides. In this paper, the sorption of Endrin, a nonionic persistent organochlorine pesticide, to montmorillonite and kaolinite was investigated. The effect of pH, ionic strength on the sorption was studied. The effect of intercalation of hydroxyl aluminium species on sorption of Endrin to montmorillonite was also investigated. The results show that, the sorption isotherm of Endrin to montmorillonite and kaolinite was linear. The sorption increases with the increase in ionic strength. pH has effect on the sorption and the sorption on both montmorillonite and kaolinite has obvious troughs at pH about 7.2 and 5.4, respectively. The intercalation of hydroxyl aluminium species decreases the sorption. Sorption mechanism of Endrin to montmorillonite and kaolinite was suggested to be a combination of hydrophobic interaction and charge-dipole interaction and troughs in the effect of pH on sorption was attributed to the proton shift reaction of the broken bonds at the clay edges.

  • oxidized carbon nanotubes for simultaneous removal of Endrin and cd π from water and their separation from water
    Journal of Chemical Technology & Biotechnology, 2009
    Co-Authors: Xianjia Peng, Jianjun Jia, Zhaokun Luan
    Abstract:

    BACKGROUND: Previous investigation has shown that carbon nanotubes (CNTs) are effective for the removal of organic pollutants and oxidized carbon nanotubes (OCNTs) are effective for the removal of heavy metals. In this investigation, OCNTs were used for simultaneous removal of Endrin and Cd(II) from water. Separation of OCNTs from water was also investigated. RESULTS: The removal efficiencies of Endrin and Cd(II) by OCNTs were 89-97% and 96-100%, respectively. Endrin removal capacity of OCNTs is approximately the same as that of powdered activated carbon (PAC) and as-prepared CNTs. Cd(II) removal capacity of OCNTs is much higher than that of PAC and as-prepared CNTs. OCNTs can be separated efficiently from water using AlCl(3). CONCLUSION: OCNTs are effective for the simultaneous removal of Endrin and Cd(II) and after adsorption, OCNTs can be separated from water by dosing AlCl(3). (C) 2008 Society of Chemical Industry

S. J. Stohs - One of the best experts on this subject based on the ideXlab platform.

  • protective effects of lazaroid u74389f 16 desmethyl tirilazad on Endrin induced lipid peroxidation and dna damage in brain and liver and regional distribution of catalase activity in rat brain
    Free Radical Biology and Medicine, 1995
    Co-Authors: M. Bagchi, E. A. Hassoun, D. Bagchi, S Ghosh, S. J. Stohs
    Abstract:

    Abstract Endrin, a poly-halogenated cyclic hydrocarbon, induces hepatic lipid peroxidation, modulates calcium homeostasis, decreases membrane fluidity, and increases nuclear DNA damage. Little information is available on the neurotoxicity of Endrin. The effects of Endrin on lipid peroxidation, DNA damage, and regional distribution of catalase activity were assessed in rat brain and liver 24 h following an acute oral dose of 4.5 mg Endrin/kg. Lipid peroxidation associated with whole brain mitochondria increased 2.4-fold, whereas microsomal lipid peroxidation increased 2.8-fold following Endrin administration. Lipid peroxidation also increased 2.0-fold both in hepatic mitochondria and microsomes. Catalase activity decreased 24% in the hypothalamus, 23% in the cortex, 38% in the cerebellum, and 11% in the brain stem in response to Endrin. A 4.3-fold increase in brain nuclear DNA-single strand breaks (SSB) was observed in Endrin-treated rats. Pretreatment of rats intraperitoneally with the lazaroid U74389F (16-desmethyl tirilazad) (10 mg/kg in two doses) attenuated the biochemical consequences of Endrin-induced oxidative stress. The administration of U74389F in citrate buffer (pH 3.8) provided better protection than administering the lazaroid in corn oil, decreasing Endrin-induced lipid peroxidation by 50–80% and DNA-SSB by approximately 72% in liver and 85% in brain, while ameliorating the suppressed catalase activity. The data suggest an involvement of an oxidative stress in the neurotoxicity and hepatotoxicity induced by Endrin, which can be attenuated by the lazaroid U74389F.

  • Endrin-induced increases in hepatic lipid peroxidation, membrane microviscosity, and DNA damage in rats
    Archives of Environmental Contamination and Toxicology, 1992
    Co-Authors: M. Bagchi, E. A. Hassoun, D. Bagchi, S. J. Stohs
    Abstract:

    Endrin is a polyhalogenated cyclic hydrocarbon pesticide which produces hepatic and neurologic toxicity. Previous studies have indicated that Endrin induces hepatic lipid peroxidation. In order to further assess the possible role of lipid peroxidation in the toxicity of Endrin, the dose- and time-dependent effects of Endrin on hepatic lipid peroxidation, membrane microviscosity and DNA damage in rats were examined. Rats were treated with 0, 3.0, 4.5, or 6.0 mg Endrin/kg as a single oral dose in corn oil, and the animals were killed 0, 12, 24, 48, or 72 h post-treatment. Dose-dependent increases in hepatic mitochondrial and microsomal lipid peroxidation and microviscosity as well as nuclear DNA single strand breaks were observed as early as 12 h post-treatment. Maximum increases in these three parameters occurred 24 h after Endrin administration at all three doses. While the incidence in DNA damage decreased with time after 24 h, the incidence of lipid peroxidation and microviscosity of microsomal and mitochondrial membranes remained relatively constant. Dose- and time-dependent increases in liver and spleen weight/body weight ratios with decreases in thymus weight/body weight ratios were observed. The data indicate that Endrin administration induces hepatic lipid peroxidation which may be responsible for the increased membrane microviscosity as a result of membrane damage as well as enhanced DNA damage.

  • Endrin-induced production of nitric oxide by rat peritoneal macrophages
    Toxicology letters, 1992
    Co-Authors: P.i. Akubue, S. J. Stohs
    Abstract:

    Abstract The effect of oral Endrin administration to rats on the production of nitric oxide (NO) by peritoneal macrophages was investigated. Nitric oxide formation was measured as nitrite. Endrin (4.5 mg kg ) enhanced the secretion of NO by approx. 300%. The effect of Endrin on NO formation was both dose- and time-dependent. Ellagic acid, which has been shown to be a potent antioxidant, inhibited the elevation of NO production induced by Endrin. These results suggest that the toxicity of Endrin may at least in part be due to the production of an oxidative stress.

  • Effect of Endrin on the hepatic distribution of iron and calcium in female Sprague-Dawley rats.
    Journal of biochemical toxicology, 1992
    Co-Authors: Debasis Bagchi, E. A. Hassoun, Manashi Bagchi, S. J. Stohs
    Abstract:

    The distribution of iron and calcium in hepatic subcellular fractions of female rats treated with Endrin (1, 2, 3, 4, 10, 10-hexachloro-6, 7-epoxy-1, 4, 4α, 5, 6, 7, 8, 8α-octahydroendo, endo-1, 4:5, 8-dimethanonaphthalene) was determined. Endrin in corn oil was administered orally to rats in single doses of 3, 4.5, or 6 mg/kg, and the animals were killed at 0, 12, 24, 48, or 72 hr posttreatment. Iron and calcium were determined by atomic absorption spectroscopy. The administration of Endrin increased the iron content of mitochondria and decreased the iron content of microsomes and nuclei. Significant increases occurred in the calcium content of mitochondria, microsomes, and nuclei. Thus, the results indicate that with respect to the subcellular distribution of iron and calcium, Endrin produces differential effects. Vitamin E succinate administration partially prevented the Endrin-induced hepatic alterations in iron and calcium homeostasis. Endrin also produced dose- and time-dependent increases in the liver and spleen weight/body weight ratios, while decreasing the thymus weight/body weight ratios. The altered distribution of calcium and iron may contribute to the broad range of effects of Endrin.