Molecular & Cellular Toxicology

Park, Jinah; Kim, Seoyun; Song, Jisoo; Lim, Whasun

doi: 10.1007/s13273-026-00639-1pmid: N/A

BackgroundClimate change-driven heat stress is an emerging toxicological stressor that disrupts thermoregulation and endocrine function, impairing livestock fertility across the reproductive lifespan.ObjectiveThis review aims to synthesize mechanistic evidence linking heat stress to female reproductive dysfunction in cattle, pigs, and poultry.ResultsGrowing evidence indicates that climate change-associated heat stress compromises female reproduction in cattle, pigs, and poultry. In cattle, chronic heat stress perturbs the hypothalamic–pituitary–gonadal and stress axes, induces oxidative and mitochondrial damage in gametes and embryos, and disrupts uterine signaling, thereby impairing implantation and maternal recognition of pregnancy. In pigs, impaired heat dissipation, negative energy balance, and uterine and placental injury converge to reduce fertility and compromise pregnancy maintenance. In poultry, heat stress alters neuroendocrine and intestinal functions and diverts energy away from reproduction, leading to sustained declines in laying performance and egg quality.ConclusionThese findings highlight heat stress as a multidimensional reproductive toxicant in livestock and the need to evaluate its cumulative impact on fertility under climate warming.

Hong, Hyehyun; Choi, Byeong-Min; Kim, Minkyeong; Kim, Changmu; Park, Jin-Soo; Chi, Won-Jae; Kim, Seung-Young

doi: 10.1007/s13273-026-00635-5pmid: N/A

BackgroundAging-associated muscle decline is closely associated with oxidative stress-induced apoptosis and chronic inflammatory signaling. Excessive accumulation of reactive oxygen species disrupts cellular redox homeostasis and promotes mitochondrial dysfunction, ultimately leading to myocyte apoptosis and muscle degeneration. In addition, inflammatory mediators and cytokine signaling pathways further amplify oxidative damage and contribute to progressive muscle deterioration.ObjectiveThis study evaluated the biological effects of the mycelial culture filtrate of Trametes suaveolens KMRB 17121435 (Ts_MY) on oxidative stress-associated cytotoxicity in C2C12 myoblasts and inflammatory responses in lipopolysaccharide-stimulated RAW 264.7 macrophages.ResultsUnder H2O2 exposure, Ts_MY treatment increased C2C12 cell viability in a concentration-dependent manner and modulated apoptosis-related regulators, including decreased Bax expression, increased Bcl-2 levels, reduced caspase-9 and caspase-3 cleavage, and attenuated PARP cleavage. In RAW 264.7 macrophages, Ts_MY exhibited no cytotoxicity within the tested concentration range and significantly suppressed nitric oxide and prostaglandin E2 production. Ts_MY also reduced the expression of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), accompanied by decreased inducible nitric oxide synthase and cyclooxygenase-2 expression and inhibition of NF-κB signaling. Radical scavenging activity was confirmed using ABTS and DPPH assays. LC–MS/MS profiling tentatively indicated the presence of phenolic and aromatic metabolites, including protocatechuic acid-related signals based on accurate mass and database matching.ConclusionThese findings demonstrate that Ts_MY modulates oxidative stress- and inflammation-associated cellular responses in vitro through regulation of apoptosis-related signaling and NF-κB-mediated inflammatory pathways. Because all experiments were conducted in cell-based systems, further studies are required to identify active constituents and validate their biological effects in more complex models.