Protective Effects of Gallic Acid Against Lead Acetate- Induced Toxicity in Mice Ovary: Focus on Apoptosis,...

Lead is an environmental pollutant recognized for its toxicity to the reproductive system. This study investigated the effects of gallic acid (GA), a polyphenolic compound found in plants, on the ovaries of mice exposed to lead (Pb) in the form of lead acetate. Forty Balb/c mice were divided into five groups: control (no treatment), sham (normal saline), GA (75 mg/kg), Pb (30 mg/kg), and GA (75 mg/kg) + Pb (30 mg/kg). Daily treatments were administered for 35 days via oral gavage, after which the ovaries were examined. The mRNA expression of antioxidant, inflammatory, and apoptotic genes as well as two microRNAs (miRs) involved in folliculogenesis, was measured using real-time reverse transcription polymerase chain reaction (RT-PCR). The results of RT-PCR indicated that Pb increased the expression of miR-132, Il-1β (Interleukin-1 beta), Tnf-α (Tumor necrosis factor alpha), P53 (Tumor protein 53), Caspase-3 (p ≤ 0.05), and Nf-κB (Nuclear factor kappa-light-chain-enhancer of activated B cells) compared to the control group significantly (p ≤ 0.01). Pb remarkably reduced the expression of Vegf (Vascular endothelial growth factor) compared to the sham group (p ≤ 0.05). GA elevated the expression of miR-125b, Gpx (Glutathione peroxidase), and Gr (Glutathione reductase) compared to the control group, while also increasing the expression of Bcl-2 (B-cell lymphoma 2 apoptosis regulator) compared to the sham group, all of them statistically significant (p ≤ 0.05). In the (GA + Pb) group, GA increased the expression of miR-125b, Bcl-2, and Vegf, while it decreased the expression of Caspase-3 compared to the Pb group significantly (p ≤ 0.05). In summary, exposure to lead acetate (Pb) demonstrates detrimental effects on ovarian function by reducing antioxidant capacity and inducing inflammation and apoptosis. In contrast, gallic acid (GA) plays a protective role and mitigates the harmful effects of lead on the ovaries.