Carbonyl sulfide exposure induces mitochondrial impairment by disrupting energy metabolism in Tribolium castaneum (Herbst)

Carbonyl sulfide (COS) has recently emerged as a promising alternative to phosphine (PH₃) for managing stored-product insect pests, yet its subcellular mechanisms of toxicity remain poorly understood. In this study, we performed transmission electron microscopy (TEM), mitochondrial complex activity and antioxidant enzyme activity assays to investigate the mitochondrial toxicity and oxidative stress response induced by COS fumigation in Tribolium castaneum. COS exposure significantly altered mitochondrial ultrastructure, as demonstrated by matrix rarefaction, and vacuolization. These structural disruptions were accompanied by a decline in ATP content, suggesting impaired oxidative phosphorylation (OXPHOS). Notably, the NAD⁺ levels increased without significant changes in NADH and NAD⁺/NADH ratio, indicating modulation of NAD⁺ homeostasis under COS-induced stress. Biochemical analysis revealed inhibition of Complex III activity, with compensatory upregulation of Complex II (succinate dehydrogenase, SDH) and Complex IV (cytochrome c oxidase, COX), suggesting a disrupted but adaptive mitochondrial response. Furthermore, COS exposure disrupted antioxidant enzyme activities, where superoxide dismutase (SOD) remained unchanged, while peroxidase (POD) was significantly elevated and catalase (CAT) activity was suppressed, indicating dysregulation of antioxidant defenses. These findings suggest that COS compromises mitochondrial energy metabolism and modulates redox homeostasis, likely contributing to oxidative damage and cellular dysfunction. This is the first comprehensive study of COS-induced mitochondrial and antioxidant responses, offering novel insights into its toxic mode of action and supporting its potential utility as an effective fumigant against T. castaneum.