Ecotoxicology and environmental safetySep 18, 2026

T-2 toxin may cause cartilage cell damage by affecting energy production controlled by SIRT1 and PGC-1α

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Sep 19, 2026

Abstract

T-2 toxin causes significant mitochondrial dysfunction in chondrocytes, evidenced by a loss of mitochondrial membrane potential and reduced mitochondrial DNA copy number.

Chondrocytes exposed to T-2 toxin displayed ultrastructural mitochondrial abnormalities and injury.
T-2 toxin decreased the expression of Sirtuin 1 (SIRT1) and increased acetylation of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α).
Downregulation of proteins involved in mitochondrial biogenesis was observed following T-2 toxin exposure.
Activation of SIRT1 with resveratrol partially restored mitochondrial biogenesis and reduced chondrocyte injury.
These results suggest that the SIRT1/PGC-1α pathway may play a role in T-2 toxin-induced mitochondrial impairment.

Simplified

T-2 toxin, a type A trichothecene mycotoxin, has been implicated as an environmental risk factor for Kashin-Beck disease (KBD), an endemic osteoarthropathy characterized by cartilage damage. However, whether T-2 toxin impairs mitochondrial biogenesis in chondrocytes and the underlying regulatory mechanism remain unclear. This study investigates the effects of T-2 toxin on mitochondrial function and biogenesis using in vivo and primary chondrocyte models and evaluated the involvement of the SIRT1/PGC-1α signaling pathway. T-2 toxin induced chondrocyte injury and mitochondrial dysfunction, as evidenced by ultrastructural mitochondrial abnormalities, loss of mitochondrial membrane potential (ΔΨm), and reduced mitochondrial DNA copy number (mtDNAcn). T-2 toxin also decreased Sirtuin 1 (SIRT1) protein expression, increased peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) acetylation, and downregulated proteins involved in mitochondrial biogenesis. Pharmacological activation of SIRT1 with resveratrol partially restored PGC-1α deacetylation and mitochondrial biogenesis and attenuated chondrocyte injury. These findings indicate that suppression of SIRT1/PGC-1α pathway contributes to T-2 toxin-induced impairment of mitochondrial biogenesis and chondrocyte injury. This study provides mechanistic evidence linking T-2 toxin exposure to defective mitochondrial biogenesis in chondrocytes and identifies the SIRT1/PGC-1α axis as a potential target for mitigating T-2 toxin-induced cartilage toxicity.

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T-2 toxin may cause cartilage cell damage by affecting energy production controlled by SIRT1 and PGC-1α

Abstract

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