Taurine alleviated acrylamide-induced ovarian toxicity via suppression of oxidative stress and apoptosis in mice
- PMID: 40250412
- DOI: 10.1177/07482337251335541
Taurine alleviated acrylamide-induced ovarian toxicity via suppression of oxidative stress and apoptosis in mice
Abstract
Acrylamide (Acr) poses reproductive toxicity risks to humans due to its ability to penetrate cell membranes and disrupt cellular balance. Taurine (Tau), a sulfur-containing amino acid with cell membrane stabilization and antioxidant properties, may mitigate these effects. This study examined how Tau can protect against oxidative stress and apoptosis induced by Acr in mouse ovarian tissue. Forty adult healthy mice, aged 6-8 weeks, were randomly assigned to four groups including the controls (received normal saline orally), Acr (50 mg/kg/day Acr orally), Acr + Tau75 (Acr and 75 mg/kg/day Tau), and Acr + Tau150 (Acr and 150 mg/kg/day Tau). Treatments were administered for 35 days, followed by assessments of stress markers and apoptosis via immunofluorescence and TUNEL assays. Both doses of Tau significantly increased the gene and protein expression levels of stress response enzymes, including Gpx1, Sod1, and Cat. Moreover, Tau significantly decreased the gene expression levels of apoptotic markers Caspase3 and Bax, while upregulating the antiapoptotic gene Bcl2l2. The TUNEL assay revealed the preventive properties of Tau against Acr-induced apoptosis in the ovaries. The current findings suggest the promising properties of Tau in the prevention of Acr-induced oxidative stress and apoptosis in mouse ovarian tissue. Therefore, Tau could play a protective role against Acr-induced reproductive toxicity in females, meriting further research into its potential applications.
Keywords: Reproductive toxicity; apoptosis; female; ovary; oxidative stress; taurine.
Conflict of interest statement
Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Research Materials
Miscellaneous
