Cadmium exposure accelerates ovarian aging in broiler breeders through oxidative stress and inflammation

Abstract

Cadmium (Cd) is an environmental pollutant with reproductive toxicity. Until now, its effects on ovarian aging of broiler breeders remain poorly understood. This study established a 10-week Cd exposure model in broiler breeders. The data indicated that Cd administration impaired the laying performance and compromised the egg quality. Notably, it markedly elevated the enzymatic activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the serum while concurrently reducing serum TG concentration (P < 0.05). Meanwhile, Cd exposure decreased the relative weight of ovarian stroma, induced the damage to the ovarian tissue structure, and significantly reduced the follicle number (P < 0.05). Furthermore, Cd exposure triggered ovarian oxidative stress, manifested by elevated 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA) content and diminished antioxidant capacity (T-AOC, SOD, GSH-Px) (P < 0.05). It also promoted the transcriptional activation of pro-inflammatory genes (IFN-γ, IL-8, IL-17, NF-κB) (P < 0.05). TUNEL staining and RT-qPCR analysis revealed that Cd exposure increased ovarian cell apoptosis rates and upregulated the mRNA expression of pro-apoptotic genes, including Bax, caspase-3, caspase-8, and caspase-9 (P < 0.05). Additionally, immunofluorescence and RT-qPCR results further confirmed that Cd exposure upregulated the senescence-associated marker P21 at both the protein and transcriptional levels, while upregulating the mRNA expression of P16 and γ-H₂AX, and downregulating the mRNA expression levels of senescence-regulating genes SIRT1 and SIRT6 (P < 0.05). In conclusion, Cd exposure accelerates ovarian aging in broiler breeders by inducing oxidative stress and fostering inflammation, which provides potential therapeutic targets for mitigating Cd-induced ovarian aging.