Early oxidative stress in testis and epididymal sperm in streptozotocin-induced diabetic mice: Its progression and genotoxic consequences

Balakrishna, Shrilatha; Muralidhara, .

doi:10.1016/j.reprotox.2007.02.001

Cited by 203 publications

(154 citation statements)

References 47 publications

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“…Hence it can be reasonably postulated that abnormalities observed in this study is caused by STZ itself. While STZ is a well-known genotoxic agent in cell model, and it has been shown to causes significant oxidative impairments in the male reproductive milieu during early diabetic phase in mice [22]. The rapid decline in testosterone level and increase in sperm DNA damage during first 36 days in this study also confirms the direct effect of STZ rather than hyperglycemia induced response.…”

Section: Discussionsupporting

confidence: 75%

Germ cell abnormalities in streptozotocin induced diabetic mice do not correlate with blood glucose level

Bose

Adiga

D’Souza

et al. 2012

J Assist Reprod Genet

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Purpose To assess the effect of streptozotocin induced hyperglycemia on germ cell integrity, DNA ploidy and methylation status for a period of two spermatogenesis cycles in adult male Swiss albino mice. Methods Streptozotocin injected mice were monitored for hyperglycemia at a regular interval for a period of 36 and 72 days. The DNA integrity in epididymal spermatozoa was determined by the comet assay. Flow cytometric analysis was done in germ cells to assess the DNA ploidy. The global methylation analysis in germ cells was done by 5-methyl cytosine immunostaining.Results Streptozotocin administration successfully resulted in hyperglycemic response which significantly affected serum testosterone level, sperm DNA integrity and DNA ploidy at the end of 36 days. However, no changes were observed in either epididymal sperm concentration or germ cell methylation status. In contrast, at the end of 76 days, although serum testosterone level, sperm DNA integrity and DNA ploidy status were unperturbed significantly in hyperglycemic group, the epididymal sperm concentration and methylation status of preleptotene/zygotene cells were significantly altered. Importantly, an attempt to find out the association between the blood glucose levels and the abnormalities in hyperglycemic group failed to demonstrate any correlation. Conclusions The germ cell abnormalities observed in hyperglycemic group could be interpreted as a primary effect of streptozotocin and not due to hyperglycemia. Our results call for further evaluation of streptozotocin before its application to study the hyperglycemic responses on male germ cells.

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Section: Discussionsupporting

confidence: 75%

Germ cell abnormalities in streptozotocin induced diabetic mice do not correlate with blood glucose level

Bose

Adiga

D’Souza

et al. 2012

J Assist Reprod Genet

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“…Oxidative stress is known to play an important role in various manifestations of MetS, but one that is thought to be only an early event in the pathology of what are chronic diseases (Roberts & Sindhu 2009). In diabetes, there is evidence both in men and in animal models, whether spontaneously occurring (O'Neill et al 2009) or chemically induced diabetic mice (Shrilatha & Muralidhara 2007a, O'Neill et al 2009) and rats (Shrilatha & Muralidhara 2007b), that the condition is associated with marked increases in oxidative stress and sperm nDNA damage. Hyperglycaemia is known to cause oxidative stress (Wautier & Schmidt 2004, Chekir et al 2006 and to accelerate the accumulation of advanced glycation end products and their receptor RAGE, both of which are capable of generating, promoting and/or amplifying oxidative stress and its detrimental consequences.…”

Section: Discussionmentioning

confidence: 99%

Spermatogenic and sperm quality differences in an experimental model of metabolic syndrome and hypogonadal hypogonadism

Mallidis¹,

Czerwiec²,

Filippi³

et al. 2011

Reproduction

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The synergistic effect of the co-morbidities that comprise metabolic syndrome (MetS) is increasingly being recognised as an important contributor in the pathology of a broad spectrum of seemingly disparate conditions. However, in terms of male reproductive function, beyond erectile dysfunction, little is known about the influence of this cohort (collectively or separately) on spermatogenesis and sperm quality. The aims of this study were to assess the reproductive tract of a MetS animal model for detrimental changes, to determine whether a group of compounds (advanced glycation end products and their receptor) known to cause cell dysfunction and DNA damage was present and assess whether hypogonadotropic hypogonadism was the main contributing factor for the changes seen. Animals fed a high-fat diet were found to have significantly increased cholesterol, triglycerides, blood glucose, mean arterial pressure and visceral fat levels. Although serum testosterone was decreased, no changes were seen in either testicular or epididymal histology. Immunolocalisation of N 3 -carboxymethyl-lysine and the receptor for advanced glycation end products was found in the testes, epididymides and sperm of the two treated groups of animals; however, ELISA did not show any difference in protein levels. Similarly, assessment of sperm nuclear DNA (nDNA) fragmentation by acridine orange test did not find significant differences in nDNA integrity. We conclude that the minimal effect on spermatogenesis and sperm quality seen in our model is probably due to the moderate increase of blood glucose rather than the hypogonadism.

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“…16 Measurement of oxidative stress markers Oxidative stress markers were quantified in both testis cytosol and mitochondria as described earlier from our laboratory. 10,11 For determination of reactive oxygen species, testis cytosol/mitochondrial protein (0.2 mg) suspended in Locke's solution was incubated with dihydrodichlorofluorescein diacetate (5 mM) for 30 min at room temperature. The fluorescence intensity measured at excitation (488 nm) and emission wavelengths (530 nm) were quantified from a dichlorofluorescein standard curve.…”

Section: Methodsmentioning

confidence: 99%

“…9 Our recent findings in STZ-diabetic adult rodent models have shown the occurrence of oxidative stress in the testis during acute phase and its progression. 10,11 However, to the best of our knowledge, no data exist on the vulnerability of an immature (prepubertal) testis to oxidative stress under experimentally induced diabetes. Owing to the phenomenal increase in the incidence of diabetes among children/adolescent males, comprehensive studies are warranted to understand the nature/ extent of oxidative impairments and associated biochemical dysfunctions in immature testis.…”

Section: Introductionmentioning

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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Early oxidative stress in testis and epididymal sperm in streptozotocin-induced diabetic mice: Its progression and genotoxic consequences

Cited by 203 publications

References 47 publications

Germ cell abnormalities in streptozotocin induced diabetic mice do not correlate with blood glucose level

Germ cell abnormalities in streptozotocin induced diabetic mice do not correlate with blood glucose level

Spermatogenic and sperm quality differences in an experimental model of metabolic syndrome and hypogonadal hypogonadism

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

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