Polystyrene microplastics induce apoptosis in chicken testis via crosstalk between NF-κB and Nrf2 pathways.

Microplastics (MPs) are a new type of pollutants that are widespread in nature, and their toxic effects on humans or animals are receiving attention. Birds are in a higher ecological niche in nature, and MPs may have potential bioaccumulation and biomagnification risks to birds. The mechanisms underlying the reproductive toxicity of MPs to birds are mainly unknown. To study the reproductive toxicity of MPs to birds, we randomly divided chickens into six groups and exposed polystyrene microplastics (PS-MPs) through drinking water (0, 1, and 100 mg/L) for 28 and 42 days. We found that PS-MPs caused testicular inflammatory infiltration and interstitial hemorrhage, resulting in testicular tissue damage; the expression of Claudin3 and Occludin in the blood-testis barrier (BTB) decreased and may damage the integrity of the BTB. PS-MPs exposure inhibited the expression of the Nrf2-Keap1 pathway, which in turn reduced HO-1 and NQO1, simultaneous GSH and T-AOC were also reduced, resulting in an imbalance of the redox system; in addition, the NF-κB signaling pathway was activated, increasing the expression of TNF-α, COX-2 and iNOS. Under redox system imbalance and inflammatory stress, exposure to PS-MPs led to decreased expression of Bcl-2 and increased Bax, cytc, caspase-8, and caspase-3, etc., activating apoptosis, and ultimately causing testicular damage. These results suggested that PS-MPs exposure led to an imbalance of the redox system and an inflammatory response, inducing both endogenous and exogenous apoptosis, resulting in testicular tissue damage. Our study provides a theoretical basis for reproductive injury mechanisms in chicken.