The productivity of dairy animals has significantly increased over the past few decades due to intense genetic selection. However, the enhanced yield performance of milk animals caused a proportional increase in stress and compromised reproductive efficiency. Optimal reproductive performance is mandatory for the sustainable production of dairy animals. Reproductive efficiency is marked by proper estrus detection and precise breeding to achieve maximum pregnancies. The existing conventional methods of estrus detection are somewhat labor intensive and less efficient. Similarly, the modern automated methods that rely on detecting physical activity are expensive, and their efficiency is affected by factors such as type of housing (tie stall), flooring, and environment. Infrared thermography has recently emerged as a technique that does not depend on monitoring physical activity. Furthermore, infrared thermography is a non-invasive, user-friendly, and stress-free option that aids in the detection of estrus in dairy animals. Infrared thermography has the potential to be considered a useful non-invasive tool for detecting temperature fluctuations to generate estrus alerts without physical contact in cattle and buffaloes. This manuscript highlights the potential use of infrared thermography to understand reproductive physiology and practical implementation of this technique through discussing its advantages, limitations, and possible precautions.

Inflammation disrupts the normal function of granulosa cells (GCs), which leads to ovarian dysfunction and fertility decline. Inflammatory conditions such as polycystic ovary syndrome (PCOS), primary ovarian insufficiency (POI), endometriosis, and age-related ovarian decline are often associated with chronic low-grade inflammation. Nicotinamide mononucleotide (NMN) is an important precursor of NAD⁺ and has gained attention for its potential to modulate cellular metabolism, redox homeostasis, and mitigate inflammation. This study investigated the protective roles of NMN against lipopolysaccharide LPS-mediated inflammation in GCs. The results of this experiment demonstrated that LPS had negative effects on GCs in term of reduced viability and proliferation rates and upregulated the production of pro-inflammatory cytokines, including interleukin-1 beta (IL-1β), interleukin-6 (IL-6), cyclooxygenase-2 (Cox-2), and tumor necrosis factor-alpha (TNF-α). Notably, the levels of NAD⁺ and NAD⁺/NADH ratio in GCs were reduced in response to inflammation. On the other hand, NMN supplementation restored the NAD⁺ levels and the NAD⁺/NADH ratio in GCs and significantly reduced the expression of pro-inflammatory markers at both mRNA and protein levels. It also enhanced cell viability and proliferation rates of GCs. Furthermore, NMN also reduced apoptosis rates in GCs by downregulating pro-apoptotic markers, including Caspase-3, Caspase-9, and Bax while upregulating anti-apoptotic marker Bcl-2. NMN supplementation significantly reduced reactive oxygen species ROS and improved steroidogenesis activity by restoring the estradiol (E2) and progesterone (P4) levels in LPS-treated GCs. Mechanistically, this study found that NMN suppressed the activation of the TLR4/NF-κB/MAPK signaling pathways in GCs, which regulates inflammatory processes. In conclusion, the findings of this study revealed that NMN has the potential to reduce LPS-mediated inflammatory changes in GCs by modulating NAD⁺ metabolism and inflammatory signaling pathways. NMN supplementation can be used as a potential therapeutic agent for ovarian inflammation and related fertility disorders.

The decline in female fecundity is linked to advancing chronological age. The ovarian reserve diminishes in quantity and quality as women age, impacting reproductive efficiency and the aging process in the rest of the body. NAD⁺ is an essential coenzyme in cellular energy production, metabolism, cell signaling, and survival. It is involved in aging and is linked to various age-related conditions. Hallmarks associated with aging, diseases, and metabolic dysfunctions can significantly affect fertility by disturbing the delicate relationship between energy metabolism and female reproduction. Enzymes such as sirtuins, PARPs, and CD38 play essential roles in NAD⁺ biology, which actively consume NAD⁺ in their enzymatic activities. In recent years, NAD⁺ has gained much attention for its role in aging and age-related diseases like cancer, Alzheimer’s, cardiovascular diseases, and neurodegenerative disorders, highlighting its involvement in various pathophysiological processes. However, its impact on female reproduction is not well understood. This review aims to bridge this knowledge gap by comprehensively exploring the complex interplay between NAD⁺ biology and female reproductive aging and providing valuable information that could help develop plans to improve women’s reproductive health and prevent fertility issues.

This study was designed to explore the potential of infrared thermography (IRT) as an alternate approach for early pregnancy diagnosis in buffaloes. The surface temperature (ST) of different regions (eyes, muzzle, flanks, and vulva) was determined in 27 buffaloes using IRT from the day of artificial insemination (AI; Day 0), and measurement was repeated every fourth day until Day 24 post-AI. From all regions, the ST in each thermograph was recorded at three temperature values (maximum, average, minimum). Pregnancy status was confirmed through ultrasonography on Day 30, and animals were retrospectively grouped as pregnant or non-pregnant for analysis of thermographic data. In pregnant buffaloes, all three values of ST were significantly greater (p ≤ 0.05) for the left flank, while, in the left eye and vulva, only the maximum and average values were significantly greater. By contrast, the maximum ST of the muzzle was significantly lower (p ≤ 0.05) in pregnant buffaloes compared to non-pregnant buffaloes. However, the ST of the right eye and right flank did not show significant temperature variation at any value. These findings suggest that IRT has the potential to identify thermal changes associated with pregnancy in buffaloes at an early stage.

The intestinal epithelium serves as a frontline defense against dietary contaminants, such as Ochratoxin A (OTA), a mycotoxin linked to oxidative stress and cell death. OTA Toxicity is well documented; however, the epigenetic mechanisms driving its effects through chromatin remodeling and histone H3K27ac modifications remain poorly understood. We demonstrated that OTA-induced oxidative stress in porcine intestinal epithelial cells (IPEC-J2) promotes ferroptosis, a lipid peroxidation-driven cell death, through epigenomic dysregulation. Multi-omics profiling (RNA-seq, ATAC-seq, and H3K27ac CUT&Tag) showed extensive chromatin and transcriptional changes: 84,744 differentially accessible regions (51,653 open; 33,091 closed) mapping to 13,828 genes, and 19,075 dynamic H3K27ac cis-regulatory elements (8923 upregulated; 10,152 downregulated) linked to 5783 and 3198 genes, respectively. Integrative analysis identified 2622 genes with coordinated shifts in expression, accessibility, and histone marks; 822 were upregulated with enhanced promoter/enhancer activity, whereas 1800 were downregulated with epigenetic silencing. Ferroptosis-related pathways, including lipid peroxidation, iron metabolism, and PUFA metabolism, were enriched. OTA-treated cells exhibited increased levels of reactive oxygen species, lipid peroxides, and cell death (p ≤ 0.05). Cross-referencing FerrDb revealed 89 ferroptosis-associated genes, including upregulated effectors CYLD, PLA2G4α, ALOX15, and TP53, showed greater chromatin accessibility and active marks; antioxidant genes such as GCLC and SLC1A5 were repressed with chromatin closure, SCD shown same trend. Motif enrichment analysis implicated SP2, ATF3, CREB5, and ETV4 in initiating epigenetic reprogramming. Notably, ETV4 acts as a repressor of SLC39A13, disrupting metal homeostasis and promoting calcium-dependent lipid peroxidation via cPLA2-ALOX15. ETV4 knockdown increased SLC39A13 expression, reversing OTA-induced repression. These findings demonstrate that OTA triggers ferroptosis through epigenomic remodeling, linking chromatin state changes to disrupted metal homeostasis and calcium-dependent lipid peroxidation, and positioning ferroptosis as a therapeutic target against OTA-induced intestinal injury.