Article

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

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

ABSTRACT

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.

Download full-text

Full-text

Available from: Luna Samanta, Dec 27, 2015
  • Source
    • "Ethanol accumulation of hydrocarbons in membranes between fatty acid residues and between opposing monolayers (Sikkema et al., 1995) membrane toxicity in microorganisms (Sikkema et al., 1995) sudden death following recreational inhalation of propane, »-butane or iso­ butane (Rohrig, 1997) generation of hydroxyl radical in fresh meat (Karam and Simic, 1989) euphoria, sudden death, injury to liver, kidneys and brain (Flanagan and Ives, 1994) superoxide by autoxidation of ubisemiquinone in isolated mitochondria (Nohl et al., 1996) membrane derangement and proton penetration (Sikkema et al., 1992) enhanced alkylhydroperoxide reductase subunit C (AhpC) activity in resistant Escherichia coli (Ferrante et al., 1995) hemolysis in ponies (Paradis et al., 1991) induction of AhpC in E. coli K12 and overproduction of A hpC in indoleresistant E. coli variant (G arbe et al., 2000a) generates active oxygen and superoxide (Kodama et al., 1997) induction of superoxide dismutase in E. coli (Zhang and Yonei, 1991) membrane derangement and lysis of human erythrocytes (Verma and Singhal, 1991) lipid peroxidation in rat testes (Samanta et al., 1999) neuroactive PCBs disruptive of mitochondrial oxidative energy production (Maier et al., 1994) neuroactive PCBs produced oxidants in rat synaptosomes (Voie and Fonnum, 2000) euphoria, sudden death, injury to liver, kidneys and brain (Flanagan and Ives, 1994) vasodilation, cardiac arrest (sudden death), hemolytic anemia (reviewed by Tse et al., 1990) lipid peroxidation (Channel et al., 1998, Toraason et al., 1999, Plaa, 2000) oxidative DNA damage (Toraason et al. 1999) alteration of mitochondrial structure by chloroform (Guastadisegni et al., 1999) generation of hydroxyl radical in white and red muscle meat (Karam and Simic, 1990) euphoria, nitric oxide release causative of smooth muscle relaxation and N-nitrosamine formation, methemoglobinemia (Maikel, 1988; Hecht, 1997) lipid peroxidation in liver, lung and kidney of rats (Kim et al., 1998) alcohol dehydrogenase-dependent oxidation to formic acid causative of acidosis and ocular toxicity interacts with lipid membranes at the hydrophilic head, impairs the membrane-w ater interaction and destabilises the membrane (Ueda and Yoshida, 1999) increases saturation of mitochondrial fatty acids (Rubin and Rottenberg, 1982) derangement of yeast membrane is followed by proton penetration (C art­ wright et al., 1986, Leäo et al., 1984) activates the OxyR regulator in E. coli (Belkin et al., 1996) and in Salmonella (Morgan et al., 1986) induction of cytoplasmic catalase and mitochondrial Mn-superoxide dismutase in yeast (Piper, 1995) oxidants in liver, pancreatic, brain and testicular tissues of the rat (Mantle and Preedy, 1999) oxidants in a gastric mucosal cell line (Hirokawa et al., 1998) superoxide induction and lipid peroxidation in mitochondria (Kurose et al.. 1996) "
    [Show abstract] [Hide abstract]
    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.
    Full-text · Article · Jul 2001 · Zeitschrift fur Naturforschung C
  • [Show abstract] [Hide abstract]
    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.
    No preview · Article · Aug 2000 · Archives of Environmental Contamination and Toxicology
  • Source
    [Show abstract] [Hide abstract]
    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.
    Full-text · Article · Nov 2005 · Toxicology
Show more