Lead and cadmium are prevalent heavy metal toxins that contaminate the natural environment through animal husbandry and agricultural and industrial activities. Exposing dairy cows to these pollutants can have detrimental effects on milk production and quality, leading to health problems and decreasing the animals’ production performance. Therefore, investigating the distribution of lead and cadmium content and assessing the pollution levels at dairy farms are of significant theoretical and practical significance. This study determined the spatial distribution and clustering of lead and cadmium by sampling soil and feces from dairy farms in Jiangsu, China. The data obtained, in conjunction with soil data from Jiangsu Province, were used to evaluate the extent of lead and cadmium pollution at these farms. The results indicate that lead pollution levels are relatively low, whereas cadmium pollution is moderate in multiple regions. Ultimately, this study contributes to the assessment of the risks associated with lead and cadmium in dairy farming production and supports the establishment of a sustainable animal husbandry system, serving as an effective reference for subsequent ecological health farming, disease prevention, and management.

Objective: There is a strong relationship between the content of beneficial fatty acids in milk and milk fat metabolic activity in the mammary gland. To improve milk quality, it is therefore necessary to study fatty acid metabolism in bovine mammary gland tissue. In adipose tissue, peroxisome proliferator-activated receptor gamma (PPARG), the core transcription factor, regulates the fatty acid metabolism gene network and determines fatty acid deposition. However, its regulatory effects on mammary gland fatty acid metabolism during lactation have rarely been reported.Methods: Transcriptome sequencing was performed during the prelactation period and the peak lactation period to examine mRNA expression. The significant upregulation of PPARG drew our attention and led us to conduct further research.Results: According to bioinformatics prediction, dual-luciferase reporter system detection, real-time quantitative reverse transcription polymerase chain reaction and Western blotting, miR-130a and miR-130b could directly target PPARG and inhibit its expression. Furthermore, triglyceride and oil red O staining proved that miR-130a and miR-130b inhibited milk fat metabolism in bovine mammary epithelial cells (BMECs), while PPARG promoted this metabolism. In addition, we also found that the coexpression of miR-130a and miR-130b significantly enhanced their ability to regulate milk fat metabolism.Conclusion: In conclusion, our findings indicated that miR-130a and miR-130b could target and repress PPARG and that they also have a functional superposition effect. miR-130a and miR-130b seem to synergistically regulate lipid catabolism via the control of PPARG in BMECs. In the long-term, these findings might be helpful in developing practical means to improve high-quality milk.

Iodoacetic acid (IAA), a highly cytotoxic disinfection byproduct commonly detected in drinking water, poses a potential risk to female reproductive health. The direct molecular mechanisms underlying its effects on the reproductive system epithelium remain unclear. This study demonstrates that IAA induces glycational stress in primary porcine uterine (UECs) and oviduct epithelial cells (OECs), representing an early event contributing to extensive cellular toxicity. IAA exposure inhibited Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH) enzymatic activity and promoted the accumulation of advanced glycation end products (AGEs) Nε-(carboxymethyl)lysine (CML), triggering mitochondrial dysfunction, redox imbalance, calcium dyshomeostasis, and endoplasmic reticulum stress. These disturbances activated a dysregulated signaling network involving the p38 MAPK, AKT, and NF-κB pathways, ultimately causing G1/S cell cycle arrest and apoptosis. Notably, pretreatment with the AGE inhibitor pyridoxamine reduced CML accumulation, restored mitochondrial function, and alleviated apoptotic cell death. These findings identify glycational stress as a key initiating mechanism for IAA-induced reproductive epithelial toxicity, providing mechanistic insight into the potential health risks of environmental disinfection byproducts.

Post-ovulatory aging (POA) is an inevitable factor during some assisted reproduction technology procedures, and results in poor fertilization rates and impaired embryo development. This study used RNA sequencing analysis and experimental validation to study the similarities and differences between in vivo- and in vitro-matured porcine oocytes before and after POA. Differentially expressed genes (DEGs) between fresh in vivo-matured oocyte (F_vivo) and aged in vivo-matured oocyte(A_vivo) and DEGs between fresh in vitro-matured oocyte (F_vitro) and aged in vitro-matured oocyte(A_vitro) were intersected to explore the co-effects of POA. It was found that "organelles", especially "mitochondria", were significantly enriched GO terms. The expression of genes related to the “electron transport chain” and “cell redox homeostasis” pathways related to mitochondrial function significantly showed low expression patterns in both A_vivo and A_vitro groups. WGCNA analysis to explore gene expression modules specific to A_vivo. Trait-modules association analysis showed that the red modules were most associated with in vivo aging. There are a total of 959 genes in the red module, which are mainly enriched in “RNA binding”, “mRNA metabolic process”, etc. GO terms, and “spliceosome” and “nucleotide excision repair” pathways. DNAJC7, IK, and DDX18 were at the hub of the gene regulatory network. And these genes were all expressed higher in A_vivo. In summary, POA affects the organelle function of oocytes. A_vivo oocytes have some unique gene expression patterns. These genes may be potential anti-aging targets. This study helps us understand the detailed mechanism of POA and provides strategies for researching oocyte aging.

In brief: Ferroptosis and mitochondrial hyperpolarization, both linked to oxidative stress, critically compromise embryo development during in vitro culture. This study demonstrates that GRK5 inhibition induces ferroptosis and mitochondrial hyperpolarization, leading to impaired developmental capacity in porcine embryos. G-protein-coupled receptor kinase 5 (GRK5) regulates cellular processes including proliferation, differentiation, and apoptosis. This study explored the effects of double-stranded RNA microinjection and inhibitor treatment (5 and 10 μM) to suppress GRK5 expression on porcine embryo development. GRK5 inhibition impaired blastocyst development and quality, elevated p53 expression, and induced ferroptosis by reducing solute carrier family 7 member 11 and glutathione peroxidase 4. It also promoted apoptosis by downregulating B-cell lymphoma extra-large and upregulating Bcl-2 associated X. Moreover, GRK5 inhibition enhanced glutaminolysis, leading to increased adenosine triphosphate levels, mitochondrial membrane potential, and superoxide accumulation. Collectively, GRK5 inhibition increased p53 expression, induced apoptosis and ferroptosis, and promoted glutaminolysis, leading to mitochondrial hyperpolarization and impaired developmental capacity of porcine embryos.