Male-mediated dominant lethal mutations in mice following prooxidant treatment

Kumar, T. R. Santhosh; Muralidhara, .

doi:10.1016/s1383-5718(99)00085-6

Cited by 20 publications

(9 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A number of chemical components have been identified to induce oxidative stress in animal models ( [53,3,46,46,15]). TBHP is a well-known ROS inducer which has been used for induction of oxidative stress and damages in male reproductive system and spermatogenesis ( [27,26,1]). Recently, we reported an increased level of ROS, H 2 O 2 and O 2…”

Section: Discussionmentioning

confidence: 99%

TBHP-induced oxidative stress alters microRNAs expression in mouse testis

Fatemi

Sanati

Shamsara

et al. 2014

J Assist Reprod Genet

View full text Add to dashboard Cite

Purpose Reactive oxygen species (ROS) and oxidative stress is one of the main reasons of male infertility. MicroRNAs (miRNAs) regulate multiple intracellular processes. Alterations in miRNAs expression may occur in different conditions and diseases. In this study, the effect of oxidative stress induced by tertiary-butyl hydroperoxide (TBHP) on the expression of candidate miRNAs in mouse testis was investigated.Methods After determining median lethal dose (LD 50 ), TBHP was intraperitoneally (ip) injected at the dilution of 1:10 LD 50 into the adult male mice for 2weeks, and then testis tissues were removed in order to assay the ROS level. Total RNA was extracted and the expression of five miRNAs was quantified by reverse transcription-real time polymerase chain reaction (RT-qPCR).Results The flow cytometry analysis showed a significant increase in ROS level in testis. The expression of three out of five selected miRNAs, including miR-34a, miR-181b and miR-122a, showed some degrees of changes following exposure to oxidative stress. These miRNAs are involved in antioxidant responses, inflammation pathway and spermatogenesis arrest. Conclusions In conclusion, TBHP alters the miRNA expression profile of testis which might play a potential role in oxidative and antioxidative responses and spermatogenesis.

show abstract

Section: Discussionmentioning

confidence: 99%

TBHP-induced oxidative stress alters microRNAs expression in mouse testis

Fatemi

Sanati

Shamsara

et al. 2014

J Assist Reprod Genet

View full text Add to dashboard Cite

show abstract

“…At the level of the isolated spermatozoon, ROS attack can induce lipid peroxidation and DNA fragmentation disrupting both the motility of these cells and their ability to support normal embryonic development. [176][177][178][179][180][181][182] At the level of the testes, oxidative stress is capable of disrupting the steroidogenic capacity of Leydig cells 183 as well as the capacity of the germinal epithelium to differentiate normal spermatozoa. 184 A large number of independent clinical studies have demonstrated a correlative relationship between male infertility and evidence of oxidative stress in the ejaculate.…”

Section: Discussionmentioning

confidence: 99%

Antioxidant Systems and Oxidative Stress in the Testes

Aitken

Roman

2009

Advances in Experimental Medicine and Biology

162

105

View full text Add to dashboard Cite

“…Earlier, we employed sublethal dosages of hydroperoxides, such as tbHP and cumene hydroperoxide, as model pro-oxidants to induce OS in mouse testis (Rajesh Kumar and Muralidhara, 2002) and studied its genotoxic implications. Further, in adult rats, tbHP induced a significant increase in LPO and enhanced ROS generation in testis after short-term exposure (Kaur et al, 2006(Kaur et al, , 2008Kumar and Muralidhara, 1999). In the present study, tbHP, at sublethal dosages (one tenth and one fifth1/5 LD 50 /day for 3 days), induced a significant increase in LPO and enhanced ROS levels in the maternal liver and kidney, irrespective of the dosing regimen (GD 5-7 or GD 8-10 ), clearly suggesting its potential to induce OS.…”

Section: Discussionmentioning

confidence: 94%

“…This organic hydroperoxide has been previously employed as a prototypic inducer of OS in a variety of in vitro and in vivo systems (Kumar and Muralidhara, 2006;Rajesh Kumar and Muralidhara, 2002;Kaur et al, 2006Kaur et al, , 2008Kumar and Muralidhara, 1999). Before this study, tbHP has never been employed to induce OS in pregnant rodents and hence we consider this as a new experimental in vivo model.…”

Section: Introductionmentioning

confidence: 99%

Differential oxidative stress induction and lethality of rat embryos after maternal exposure tot-butyl hydroperoxide during postimplantation period

Shivananjappa

Muralidhara

2012

Drug and Chemical Toxicology

View full text Add to dashboard Cite

In mammals, reactive oxygen species (ROS) are essential factors for cell proliferation, differentiation, and growth, notably during gestation, but are also potentially damaging agents. The present study describes the extent and pattern of oxidative stress (OS) induction in maternal milieu, placenta, and embryos of rats after in vivo exposure to sublethal doses of a well-known model prooxidant, such as t-butyl hydroperoxide (tbHP). tbHP administered (intraperitoneally) to pregnant rats on specific gestation days (GDs) (either GD(5-7) or GD(8-10)) at dosages of [one tenth the median lethal dose (LD(50)) and one fifth LD(50)/day) caused significant OS, as evident by enhancement of malondialdehyde (MDA) and ROS levels, depleted reduced glutathione levels and elevated protein carbonyl content in maternal liver and kidney. Further, tbHP treatment also caused significant oxidative impairments in placenta, whereas the weights were marginally increased. Further, tbHP treatment induced a higher incidence of embryonic lethality (4- to 6-fold higher than controls) and induced marked OS among GD(13) embryos, as evidenced by elevated MDA, ROS generation, altered redox status, and enzymatic antioxidant defenses, suggesting the vulnerability of embryos. Interestingly, incidence of embryonic mortality and degree of oxidative dysfunctions caused by tbHP treatment during GD(5-7) was relatively higher, compared with GD(8-10), suggesting differential susceptibility of embryos during the early postimplantation period. Based on these findings, it is hypothesized that critical windows during early gestation may account for the differential susceptibility of developing embryos to pro-oxidants and necessitate a better understanding of this embryonic response to pro-oxidant exposures.

show abstract

Male-mediated dominant lethal mutations in mice following prooxidant treatment

Cited by 20 publications

References 24 publications

TBHP-induced oxidative stress alters microRNAs expression in mouse testis

TBHP-induced oxidative stress alters microRNAs expression in mouse testis

Antioxidant Systems and Oxidative Stress in the Testes

Differential oxidative stress induction and lethality of rat embryos after maternal exposure tot-butyl hydroperoxide during postimplantation period

Contact Info

Product

Resources

About