Olive leaf extract attenuates acrylamide-induced reproductive toxicity through reduced oxidative DNA damage and apoptosis associated with 8-OHdG and Caspase-3 in rats
Aug 2026· Journal of Molecular Histology· Vol 57· 0 citations· 63 references
Medicine
TL;DR
Investigating the protective effects of OLE against ACR-induced reproductive toxicity in male and female rats indicates that OLE exerts a significant cytoprotective effect through its antioxidant and anti-apoptotic properties, with the extent of protection varying across tissue types.
Overall, the findings indicate that Que mitigates PdCl₂-induced testicular injury, and that this protection may be associated with antioxidant, anti-inflammatory, anti-apoptotic, ER stress-related, and Nrf2/HO-1-associated responses rather than direct proof of pathway activation.
Acrylamide (Acr) is a widely encountered environmental and dietary toxicant known to induce oxidative stress and disrupt male reproductive function. Leydig cells, due to their high metabolic activity and mitochondrial dependence, are particularly vulnerable to redox imbalance. N-acetylcysteine (Nac), a thiol-containing antioxidant and glutathione precursor, has been extensively studied for its cytoprotective properties. However, its modulatory effects on Acr-induced toxicity in Leydig cells and its pharmacodynamic interaction profile remain incompletely characterized. In this study, TM3 Leydig cells were exposed to Acr in the presence or absence of Nac. Cell viability was assessed by MTT assay, and chemical interaction profiles were evaluated using ZIP, Bliss, and Chou-Talalay combination index analyses. Oxidative stress parameters, including intracellular reactive oxygen species (ROS), lipid peroxidation, antioxidant enzyme activities (SOD, CAT, GPx), and glutathione levels, were measured. Apoptotic responses were analyzed through double fluorescence staining, RT-qPCR of apoptosis-related genes (Bax, Bcl2, Casp3, Trp53), and Western blot analysis of CASP3 protein expression. Acr exposure significantly reduced cell viability, increased ROS and lipid peroxidation levels, suppressed antioxidant defenses, and activated the mitochondrial apoptotic pathway. Nac treatment markedly improved cell viability, restored antioxidant capacity, reduced oxidative stress markers, and suppressed p53/Bax/Casp3-mediated apoptotic signaling. Combination analyses revealed an antagonistic interaction profile, indicating that Nac biologically limits Acr-induced cytotoxicity. Collectively, these findings demonstrate that Nac exerts protective effects in Leydig cells by modulating redox homeostasis and mitochondrial apoptosis, suggesting its potential as a protective regulator against Acr-induced reproductive toxicity.
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