Microplastics, which are tiny plastic particles less than 5 mm in diameter, are widely present in the environment, have become a serious threat to aquatic life and human health, potentially causing ecosystem disorders and health problems. The present study aimed to investigate the effects of microplastics, specifically microplastics-polystyrene (MPs-PS), on the structural integrity, gene expression related to tight junctions, and gut microbiota in mice. A total of 24 Kunming mice aged 30 days were randomly assigned into four groups: control male (CM), control female (CF), PS-exposed male (PSM), and PS-exposed female (PSF)(n = 6). There were significant differences in villus height, width, intestinal surface area, and villus height to crypt depth ratio (V/C) between the PS group and the control group(C) (p <0.05). Gene expression analysis demonstrated the downregulation of Claudin-1, Claudin-2, Claudin-15, and Occludin, in both duodenum and jejunum of the PS group (p < 0.05). Analysis of microbial species using 16S rRNA sequencing indicated decreased diversity in the PSF group, as well as reduced diversity in the PSM group at various taxonomic levels. Beta diversity analysis showed a significant difference in gut microbiota distribution between the PS-exposed and C groups (R2 = 0.113, p<0.01), with this difference being more pronounced among females exposed to MPs-PS. KEGG analysis revealed enrichment of differential microbiota mainly involved in seven signaling pathways, such as nucleotide metabolism(p<0.05). The relative abundance ratio of transcriptional pathways was significantly increased for the PSF group (p<0.01), while excretory system pathways were for PSM group(p<0.05). Overall findings suggest that MPs-PS exhibit a notable sex-dependent impact on mouse gut microbiota, with a stronger effect observed among females; reduced expression of tight junction genes may be associated with dysbiosis, particularly elevated levels of Prevotellaceae.

Ferroptosis is a novelty form of regulated cell death, and it is mainly characterized by iron accumulation and lipid peroxidation in the cells. Its underlying mechanism is related to the amino acid, iron, and lipid metabolisms. During viral infection, pathogenic microorganisms have evolved to interfere with ferroptosis, and ferroptosis is often manipulated by viruses to regulate host cell servicing for viral reproduction. Therefore, this review provides a comprehensive overview of the mechanisms underlying ferroptosis, elucidates the intricate signaling pathways involved, and explores the pivotal role of ferroptosis in the pathogenesis of viral infections. By enhancing our understanding of ferroptosis, novel therapeutic strategies can be devised to effectively prevent and treat diseases associated with this process. Furthermore, unraveling the developmental mechanisms through which viral infections exploit ferroptosis will facilitate development of innovative antiviral agents.

Heat stress has been one of the key research areas for researchers due to the wide-ranging effects and complex mechanisms of action of its stress product reactive oxygen species (ROS). The aim of this paper is to comprehensively review and summarize the effects of heat stress on ovarian granulosa cells and their mechanism of action. We systematically reviewed the effects of heat stress on ovarian granulosa cells, including intracellular steroid hormone changes, oxidative stress, apoptosis, and mitochondrial function. Meanwhile, this paper discusses in detail several major mechanisms by which heat stress induces apoptosis in ovarian granulosa cells, such as through the activation of apoptosis-related genes, induction of endoplasmic reticulum stress, and the mitochondrial pathway. In addition, we analyzed the mechanism of ferroptosis in ovarian granulosa cells under heat stress conditions, summarized the potential association between heat stress and ferroptosis in light of the existing literature, and explored the key factors in the mechanism of action of heat stress, such as the signaling pathways of Nrf2/Keap1, HSPs, and JNK, and analyzed their possible roles in the process of ferroptosis. Finally, this paper provides an outlook on the future research direction, describing the possible interaction between heat stress and ferroptosis, with a view to providing a theoretical basis for further understanding and revealing the complex mechanism of ferroptosis occurrence in ovarian granulosa cells under heat stress.

Canthaxanthin(CX) is a ketocarotenoid, which is widely used in poultry production as a lipophilic antioxidant. Huaixiang chickens are a local breed in China famous for their excellent meat quality; improving their laying rate via nutritional regulation has attracted extensive attention. The aim of this study was to evaluate the effects of dietary CX on the laying rate and follicular development in Huaixiang hens. A total of 180 Huaixiang hens were randomly divided into five groups with six replicates, and six chickens per replication. The control group (CON) were fed a basal diet, and the treatment group (NT) were fed a basal diet supplemented with 4, 6, 8 and 10 mg/kg CX. All chickens were 26 weeks old, living at an average environmental temperature of 25 ± 2 °C with a relative humidity of 65–75%. The results showed that supplementing the CX improved the laying rate and large white follicles (LWF) number (p < 0.05) and increased the concentration of reproductive hormones (LH, FSH, E₂ and Prog) (p < 0.05), and the basal diet supplemented with 6 mg/kg CX worked best. Moreover, CX could increase the activities of antioxidant enzymes SOD and GSH-Px (p < 0.05) and reduce the content of the lipid peroxidation product MDA in Huaixiang chickens (p < 0.05); again, 6 mg/kg CX was best. In conclusion, dietary CX had positive effects on the laying rate, ovarian structure, reproductive hormone secretion, follicle development, and the antioxidant capacity of Huaixiang hens, and 6 mg/kg CX was recommended to be added to the diet of Huaixiang chickens.

The protein associated with the silencing information regulator 2-associated enzyme1 (SIRT1) is a highly conserved nicotinamide adenine dinucleotide (NAD⁺)-dependent deacetylase and a key member of the sirtuin family. SIRT1 plays an essential role in various cellular physiological processes, primarily localized in the nucleus but also active in the cytoplasm and mitochondria. Recent studies have demonstrated its capacity to delay aging in multiple organs and tissues, although its underlying mechanisms remain incompletely understood. Additionally, SIRT1 exerts a significant influence on metabolic regulation and genetic processes. As the primary source of cellular energy, mitochondria are central to numerous biological functions. Mitochondrial dysfunction has been implicated in the onset and progression of various diseases and is increasingly recognized for its role in aging-related processes. This article investigates the interaction between SIRT1 and mitochondria in regulating reproductive system aging and elucidates their potential mechanisms of action, providing insights for clinical research into reproductive system aging.

The pervasive use of plastics in numerous industrial sectors has resulted in the circulation of microplastics across diverse ecosystems and food chains, giving rise to mounting concerns regarding their potential adverse impacts on biological systems and the environment. The objective of this experiment was to investigate the distinct effects of microplastic-polyvinyl chloride (PVC) exposure on the reproductive system, intestinal tissue structure, and intestinal microbial flora of both male and female mice. A total of 24 4-week-old Kunming mice were randomly assigned to one of four groups: male control group (CM), female control group (CF), male PVC test group (PVCM), and female PVC test group (PVCF) (n = 6). The findings revealed that in terms of the reproductive system, the PVCM group exhibited an impaired testicular structure with an irregular arrangement and a significant reduction in spermatogonia, spermatocytes, and spermatozoa within the seminiferous tubules (p < 0.01). The PVCF group exhibited a notable decrease in ovarian follicles (p < 0.01), accompanied by a reduction in uterus volume, fallopian tube volume, and muscle layer thickness, all of which also decreased significantly (p < 0.01). In comparison to the control groups, exposure to PVC resulted in a reduction in the width and height of the intestinal villi, accompanied by an increase in crypt depth. This led to a significant alteration in the ratio of villus height to crypt depth (V/C) (p < 0.01). Moreover, a reduction in microbial species diversity was observed within both the PVCM and PVCF groups; additionally, it was accompanied by contrasting changes in relative abundance and functional gene profiles among the major intestinal flora constituents. In summary, the findings indicate that PVC induces damage to both male and female mice reproductive and digestive systems, further exhibiting notable sex-dependent effects on mouse intestinal microflora composition, which correlates significantly with its impact on reproductive organs.