Differential oxidative stress induction and lethality of rat embryos after maternal exposure to t-butyl hydroperoxide during postimplantation period.
Summary of "Differential oxidative stress induction and lethality of rat embryos after maternal exposure to t-butyl hydroperoxide during postimplantation period."
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.
Department of Biochemistry and Nutrition, Central Food Technological Research Institute , Mysore, Karnataka , India.
This article was published in the following journal.
Name: Drug and chemical toxicology
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/22947016
- DOI: http://dx.doi.org/10.3109/01480545.2012.710622
Medical and Biotech [MESH] Definitions
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
Agents that have a damaging effect on the HEART. Such damage can occur from ALKYLATING AGENTS; FREE RADICALS; or metabolites from OXIDATIVE STRESS and in some cases is countered by CARDIOTONIC AGENTS. Induction of LONG QT SYNDROME or TORSADES DE POINTES has been the reason for viewing some drugs as cardiotoxins.
The appearance of carbonyl groups (such as aldehyde or ketone groups) in PROTEINS as the result of several oxidative modification reactions. It is a standard marker for OXIDATIVE STRESS. Carbonylated proteins tend to be more hydrophobic and resistant to proteolysis.
A direct-acting oxidative stress-inducing agent used to examine the effects of oxidant stress on Ca(2+)-dependent signal transduction in vascular endothelial cells. It is also used as a catalyst in polymerization reactions and to introduce peroxy groups into organic molecules.
Activating Transcription Factor 3
An activating transcription factor that plays a key role in cellular responses to GENOTOXIC STRESS and OXIDATIVE STRESS.
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