Work

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

Year: 2026

Type: article

Abstract: 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 . • Carbonyl sulfide (COS) disrupts mitochondrial ultrastructure in T. castaneum . • COS exposure impairs activity of mitochondrial complexes and ATP production. • It also alters antioxidant enzyme activities involved in oxidative stress responses. • This study provides novel insights into COS-induced mitochondrial toxicity.

Source: Ecotoxicology and Environmental Safety

DOI: 10.1016/j.ecoenv.2026.119856

Authors: Na-Ri Shin, Rashmi Manohar Mahalle, Jun-Ran Kim, Bong-Su Kim, Keon Mook Seong

Institutions: Animal and Plant Quarantine Agency, Chungnam National University

Language: English

Topic: Insect Pest Control Strategies

Subfield: Plant Science

Field: Agricultural and Biological Sciences

Domain: Life Sciences

Open Access status: gold

Estimated APC paid: $3,650

Funders: Korea Advanced Institute of Science and Technology, Animal and Plant Quarantine Agency