Inhibitory effects of stress-activated nitric oxide on antioxidant enzymes and testicular steroidogenesis

Kostic, Tatjana S.; Andrić, Silvana A.; Marić, D.; Kovačević, Radmila

doi:10.1016/s0960-0760(00)00185-0

Cited by 63 publications

(31 citation statements)

References 35 publications

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“…Further, the potential contribution of stress-activated NO in regulating steroidogenesis cannot be overruled. 48 Elevation in LDH activity in the cytosol also unequivocally suggests an extensive seminiferous epithelial membrane damage and impaired spermiogenesis. 49 Earlier evidences indicate a strong correlation between diabetes and mitochondrial dysfunctions/ activation of cell death pathways.…”

Section: Discussionmentioning

confidence: 99%

Evidence of oxidative stress and mitochondrial dysfunctions in the testis of prepubertal diabetic rats

Chandrashekar

Muralidhara

2009

Int J Impot Res

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Earlier, we have shown the occurrence of oxidative impairments and their progression in the testis of diabetic adult rats. This study investigated the vulnerability of immature testis to oxidative stress and mitochondrial dysfunctions in a prepubertal (PP) diabetic rat model. PP male rats (4/6-weekold) rendered diabetic by an acute dose of streptozotocin were monitored for induction of oxidative stress in testis cytosol/mitochondria. Diabetic rats of both age groups showed severe hyperglycemia, testicular atrophy and marked oxidative damage as evidenced by enhanced generation of reactive oxygen species, hydroperoxide and malondialdehyde levels (4 week46 week). Mitochondrial dysfunctions manifested as reduction in the activities of aldehyde dehydrogenase, tricarboxylic acid cycle enzymes, enhanced activities of oxidative phosphorylation enzymes, perturbations in calcium homeostasis and membrane potential. These evidences suggest that an immature testis is vulnerable to oxidative stress under diabetes, which may play a significant role in the development of testicular degeneration, leading to impaired fertility in adulthood.

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Section: Discussionmentioning

confidence: 99%

Evidence of oxidative stress and mitochondrial dysfunctions in the testis of prepubertal diabetic rats

Chandrashekar

Muralidhara

2009

Int J Impot Res

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“…On the contrary, high levels of NO were associated with testosterone inhibition with no change in cGMP production. Additional studies found that immobilization stress increased NO in rat testis with a concomitant reduction in testosterone production (Kostic et al 1998) and that injection of an NO donor into the testis mimicked this effect (Kostic et al 2000). Furthermore, inhibiting NOS increased testosterone production in Leydig cells (Dobashi et al 2001).…”

Section: No and Steroidogenesismentioning

confidence: 95%

eNOS activation and NO function: Differential control of steroidogenesis by nitric oxide and its adaptation with hypoxia

Ducsay¹,

Myers²

2011

Journal of Endocrinology

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Nitric oxide (NO) plays a role in a wide range of physiological processes. Aside from its widely studied function in the regulation of vascular function, NO has been shown to impact steroidogenesis in a number of different tissues. The goal of this review is to explore the effects of NO on steroid production and further, to discern its source(s) and mechanism of action. Attention will be given to the regulation of NO synthases in specific endocrine tissues including ovaries, testes, and adrenal glands. The effects of hypoxia on generation of NO and subsequent effects on steroid biosynthesis will also be examined. Finally, a potential model for the interaction of hypoxia on NO synthesis and steroid production is proposed.

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“…A short, 2-h session of IMO in rats produces a sharp decline of plasma T levels and blocks the LH-induced T production in hemitestis preparations incubated in vitro, and these actions have been attributed to endogenous NO activity (29). Further studies have led to the proposal that the involvement of NO in stress is due to activation of testicular inducible nitric oxide synthase (iNOS) (30,31). In addition, multiple lines of evidence support the conclusion that IMO is associated with increased NOS mRNA and protein levels in the brain cortex (36) and paraventricular nucleus (7) and in the HPA axis (27).…”

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confidence: 99%

Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress

Weissman¹,

Sottas²,

Zhou³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Weissman BA, Sottas CM, Zhou P, Iadecola C, Hardy MP. Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress. Am J Physiol Endocrinol Metab 292: E615-E620, 2007. First published October 10, 2006; doi:10.1152/ajpendo.00412.2006.-Immobilization stress (IMO) induces a rapid increase in glucocorticoid secretion [in rodents, corticosterone CORT)] and this is associated with decreased circulating testosterone (T) levels. Nitric oxide (NO), a reactive free radical and neurotransmitter, has been reported to be produced at higher rates in tissues such as brain during stress. The biosynthesis of T is also known to be dramatically suppressed by NO. Specifically, the inducible isoform of nitric oxide synthase (iNOS) was directly implicated in this suppression. To assess the respective roles of CORT and NO in stress-mediated inhibition of T production, adult wild-type (WT) and inducible nitric oxide synthase knockout (iNOS Ϫ/Ϫ ) male mice were evaluated. Animals of each genotype were assigned to either basal control or 3-h IMO groups. Basal plasma and testicular T levels were equivalent in both genotypes, whereas testicular weights of mutant mice were significantly higher compared with WT animals. Exposure to 3-h IMO increased plasma CORT and decreased T concentrations in mice of both genotypes. Testicular T levels were also affected by stress in WT and mutant males, being sharply reduced in both genotypes. However, the concentrations of nitrite and nitrate, the stable metabolites of NO measured in testicular extracts, did not differ between control and stressed WT and iNOS Ϫ/Ϫ mice. These results support the hypothesis that CORT, but not NO, is a plausible candidate to mediate rapid stress-induced suppression of Leydig cell steroidogenesis.

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Inhibitory effects of stress-activated nitric oxide on antioxidant enzymes and testicular steroidogenesis

Cited by 63 publications

References 35 publications

Evidence of oxidative stress and mitochondrial dysfunctions in the testis of prepubertal diabetic rats

Evidence of oxidative stress and mitochondrial dysfunctions in the testis of prepubertal diabetic rats

eNOS activation and NO function: Differential control of steroidogenesis by nitric oxide and its adaptation with hypoxia

Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress

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