Age-related changes in rat testicular oxidative stress parameters by hexachlorocyclohexane

Archive für Toxikologie (Impact Factor: 5.98). 03/1999; 73(2):96-107.


Effect of repeated oral administration of hexachlorocyclohexane (HCH; 10 and 20 mg/kg body weight per day for 7, 15 and 30
days) on antioxidant defence system and lipid peroxidation (LPX) in the testis was compared between immature (15-day-old)
and mature (90-day-old) rats. In both age-groups of rats, the pesticide elicited a significant decrease in the activities
of cytosolic superoxide dismutase (SOD; total and CN−-resistant) and catalase, and ascorbic acid content together with an increase in the levels of LPX (both in crude homogenate
and subcellular fractions) and H2O2. Testicular glutathione peroxidase (GPx; total and non-selenium-dependent) activity was enhanced in both the age-groups of
rats while the testicular glutathione content as well as glutathione reductase activity remained unaltered. HCH treatment
resulted in a decrease of total epididymal sperm number with a higher incidence of dead and damaged spermatozoa, and sperms
having anomalous head. Statistical analyses suggest that the alterations in the testicular antioxidant defence profile in
the rat are not only dependent on the duration of pesticide treatment, but also influenced by age.

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    ABSTRACT: Effect of repeated oral administration of hexachlorocyclohexane (HCH) (10 and 20 mg/kg body weight/day for 7 and 30 days) on the antioxidant defense system and lipid peroxidation (LPX) of rat cerebral hemisphere (CH) was evaluated. The level of LPX was elevated after 7 days of treatment in crude homogenate (endogenous and FeSO(4)- and ascorbic acid-stimulated) and subcellular fractions except the nuclear fraction in which induction was seen after 30 days. The pesticide elicited a significant decrease in the activities of cytosolic total and CN(-)-sensitive superoxide dismutase (SOD) after 7 and 30 days of HCH treatment, but failed to evoke any change in CN(-)-resistant SOD. Catalase activity decreased throughout the treatment period. Cerebral glutathione peroxidase activity (both selenium-dependent and -independent isoenzymes) and the level of glutathione content were decreased after 7 and 30 days of treatment, respectively. Activity of glutathione reductase and content of ascorbic acid, however, were enhanced following the pesticide exposure. The results suggest that repeated HCH administration induced oxidative stress in rat CH.
    Archives of Environmental Contamination and Toxicology 08/2000; 39(1):7-12. DOI:10.1007/s002440010073 · 1.90 Impact Factor
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    ABSTRACT: Unspecific biological effects of chemically diverse solvents strikingly reveal the unifying motif of oxidant toxicity both in higher organisms and in aerobic bacteria. In a few spectacular cases, solvent metabolites with oxidant properties were demonstrated, which however cannot explain extrahepatic toxicity, e.g. in muscle and nerve cells. A common source of solvent-inducible oxidants, by contrast, is suggested to be located in mitochondria or, more general, in membranes where the respiratory chain operates. Orderly respiration depends on membrane integrity, which is invariably compromised by exposure to most solvents and many other lipophils. In rat mitochondria, toluene-induced membrane derangement has been directly implicated with superoxide production, resulting from autoxidation of the membrane-located respiratory redox-cycler ubisemiquinone. A related mechanism may occur in bacteria: Exposure of Escherichia coli to lipophils such as ethanol, tetralin, indole, chlorpromazine and procaine, or to heat shock, induces anti-oxidant proteins, which are reliable indicators of increased oxidant levels. Although many molecular details remain to be elucidated, this review documents that oxidant toxicity of lipophilic compounds is a common physiological phenomenon correlated with derangement of membranes where respiratory processes take place. Subjective consequences of acute oxidant injury are probably the hangover from alcohol and nicotine consumption, and the sudden death from recreational solvent abuse. Suggestions concerning oxidants as major contributors to ageing remain unchallenged.
    Zeitschrift fur Naturforschung C 01/2001; 56(7-8):483-91. DOI:10.1515/znc-2001-7-801 · 0.55 Impact Factor
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    ABSTRACT: Hexachlorocyclohexane (HCH), a highly persistent organochlorine insecticide, is neurotoxic at acute doses and causes degenerative effects on chronic exposure. HCH has been reported to induce oxidative stress in cells and tissues. Mammalian brain is sensitive to oxidative stress which is implicated in neurodegenerative diseases. Effect of HCH on the brain regions, cortex, cerebellum, midbrain and brainstem, has been investigated by studying the response of antioxidant enzymes in rats treated orally with HCH at 25 and 100mg/kg b.w. for 2 weeks. Lipid peroxidation and glutathione depletion was seen in all the brain regions of HCH treated rats. The brain regions showed distinct variation in the antioxidant enzyme activities. Activities of glutathione peroxidase, glutathione reductase, glutathione-S-transferase and catalase were markedly induced whereas superoxide dismutase was inhibited at higher dose in all the brain regions. Marked induction and inhibition of the antioxidant enzymes, especially in the cortex and to varying degrees in other brain regions, was seen in HCH treated rats. These biochemical changes suggest vulnerability to oxidative stress in the brain is region-specific. Whether these changes are adaptive or compromise the capacity of the brain to deal with the HCH-induced oxidative stress that could lead to degenerative neurotoxic manifestations remain to be understood.
    Toxicology 11/2005; 214(1-2):123-30. DOI:10.1016/j.tox.2005.06.005 · 3.62 Impact Factor
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