1986
DOI: 10.1016/0300-483x(86)90199-x
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Dose-dependent study of the effects of acute lindane administration on rat liver superoxide anion production, antiooidant enzyme activities and lipid peroxidation

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Cited by 72 publications
(19 citation statements)
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“…Lindane also increased lipid peroxidation and altered some antioxidant mechanisms of hepatocytes, including decreased SOD and CAT activities [143]. These changes related to oxidative stress were dose [145] and time [143] dependent, and coincided with the onset and progression of morphological lesions [143]. Studies concerning the effects of thyroid hormone on lindane hepatotoxicity showed that combined lindane-T 3 administration increased ROS production [145,146], and GSH [146] and a-tocopherol [147] depletion to an extent that exceeded the sum of the effects elicited by the separate treatments, concomitantly with extensive liver necrosis.…”
Section: Potentation Of Xenobiotic Hepatotoxicitymentioning
confidence: 97%
“…Lindane also increased lipid peroxidation and altered some antioxidant mechanisms of hepatocytes, including decreased SOD and CAT activities [143]. These changes related to oxidative stress were dose [145] and time [143] dependent, and coincided with the onset and progression of morphological lesions [143]. Studies concerning the effects of thyroid hormone on lindane hepatotoxicity showed that combined lindane-T 3 administration increased ROS production [145,146], and GSH [146] and a-tocopherol [147] depletion to an extent that exceeded the sum of the effects elicited by the separate treatments, concomitantly with extensive liver necrosis.…”
Section: Potentation Of Xenobiotic Hepatotoxicitymentioning
confidence: 97%
“…Lipid peroxidation was enhanced following exposure of rats to TCDD, organochlorines, and PCBs (e.g., Pohjanvirta et al, 1990;Junqueira et al, 1986). In lake trout, non-ortho-substituted 3,3,4,4,5-pentachlorobiphenyl (PCB 126), a stereoisomer of TCDD, caused oxidative stress detected as increased levels of microsomal lipid peroxidation and decreased content of nonenzymatic antioxidants, whereas the activities of the enzymatic antioxidants superoxide dismutase, catalase, and glutathione peroxidase were unaffected (Palace et al, 1996).…”
Section: Differences In Responses Of Biochemical Markers Of Oxidativementioning
confidence: 99%
“…The effect could be due to either a direct action of BEA or its metabolites, enzyme inactivation secondary to the higher steady-state level of reactive O 2 species underlying the oxidative stress condition induced, or both. In agreement with the latter suggestion, SOD and catalase inactivation has been reported to be produced in vitro by either superoxide radical, hydrogen peroxide, peroxyl radicals, or singlet oxygen [25][26][27], as well as in conditions undergoing severe oxidative stress in vivo [28][29][30].…”
Section: Discussionmentioning
confidence: 66%