Ivermectin impairs swine adipose tissue-derived mesenchymal stromal cells functions

Ivermectin is a versatile antiparasitic drug; however, its potential bioaccumulation in adipose tissue raises toxicological concerns regarding metabolic and reproductive health. This study evaluates the effects of Ivermectin on swine adipose tissue -derived mesenchymal stromal cells, a validated translational model. Primary adipose tissue -derived mesenchymal stromal cells isolated from porcine subcutaneous adipose tissue were exposed to clinically relevant concentrations of Ivermectin (20, 40, and 60 ng/mL) for 48 h. Cell proliferation, metabolic activity, redox balance, and adipogenic differentiation were investigated. Ivermectin exposure significantly suppressed cell proliferation via replication arrest without inducing apoptosis, while simultaneously elevating ATP production. Pharmacological stress shifted the redox balance toward a pro-oxidant state, increasing superoxide anion and nitric oxide levels, which triggered a compensatory rise in antioxidant defenses (superoxide dismutase activity and ferric reducing antioxidant power). Furthermore, Ivermectin stimulated intracellular lipid accumulation and enhanced adipogenic commitment. Ivermectin disrupts swine adipose tissue -derived mesenchymal stromal cells homeostasis by altering the redox status and promoting adipogenesis, suggesting it may act as a metabolic and cellular disruptor within the adipose cell niche.