Ferroptosis: First evidence in premature duck ovary induced by polyvinyl chloride microplastics.

Ferroptosis is frequently observed in fibrosis and diseases related to iron metabolism disorders in various mammalian organs. However, research regarding the damage mechanism of ferroptosis in the female reproductive system of avian species remains unclear. In this study, Muscovy female ducks were divided into three groups which were given purified water, 1 mg/L polyvinyl chloride microplastics (PVC-MPs) and 10 mg/L PVC-MPs for two months respectively, to investigate the ferroptosis induced by PVC-MPs caused ovarian tissue fibrosis that lead to premature ovarian failure. The results showed that the high accumulation of PVC-MPs in ovarian tissue affected the morphology and functional activity of ovarian granulosa cells (GCs) and subsequently caused the follicular development disorders and down-regulated the immunosignaling of ovarian steroidogenesis proteins 3ß-hydroxysteroid dehydrogenase (3ß-HSD), 17ß-hydroxysteroid dehydrogenase (17ß-HSD), CYP11A1 cytochrome (P450-11A1) and CYP17A1 cytochrome (P450-17A1) suggested impaired ovarian function. In addition, PVC-MPs significantly up-regulated positive expression of collagen fibers, significantly increased lipid peroxidation and malondialdehyde (MDA) level, along with encouraged overload of iron contents in the ovarian tissue were the characteristics of ferroptosis. Further, immunohistochemistry results confirmed that immunosignaling of ferroptosis related proteins Acyl-CoA synthetase (ACSL4), Cyclooxygenase 2 (COX2) and ferritin heavy chain 1 (FTH1) were significantly increased, but solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase (GPX4) were decreased by PVC-MPs in the ovarian tissue. In conclusion, our study demonstrates that PVC-MPs induced ferroptosis in the ovarian GCs, leading to follicle development disorders and ovarian tissue fibrosis, and ultimately contributing to various female reproductive disorders through regulating the proteins expression of ferroptosis.

Effect of Selenium Nanoparticles and Chitosan on Production Performance and Antioxidant Integrity of Heat-Stressed Broiler.

In this study, 336-day-old corn cob broilers were bought for the poultry experimental station during the months of May and June 2021. Before the arrival of chicks, the brooders, chick feeders, drinkers, humidity, temperature, and feeding management were controlled according to scientific patterns. These birds were randomly divided into seven groups and six replications of eight birds, viz. Group-A (positive control on basal diet only), Group-B (negative control on basal diet and HS), group-C (basal diet + simple Se 0.3 mg/kg feed), Group-D (basal diet + SeNP 0.3 mg/kg feed + HS), Group-E (BD + HS + chitosan), Group-F (BD + Se + COS), and Group-G (nano Se with chitosan 0.3 mg/kg + BD + HS). On the 42nd day of research, two birds were selected from each replication and sacrificed after blood collection. The initial data related to feeding intake, live body weight, and feed conversion ratio (FCR) were collected before slaughter. The intestinal samples were collected and immediately transferred to formalin after grass morphometry. The live body weight, FCR, feed intake, intestinal histomorphology, relative organ weight, and antioxidant parameters like MDA, SOD, and GPX were significant (P > 0.005) in all groups, with Group-G at the highest, followed by Groups-F, E, D, C, A, and B. Group-B (negative control group) was the most affected group in all aspects because of heat stress and only basal diet. It was concluded that heat stress highly causes a loss in performance, intestinal gross morphology, and histology in poultry, and increases stress conditions, whereas the selenium nanoparticle works to improve the body weight, FCR, and intestinal parameters.