High Environmental Ammonia Causes Induction in the Expression of Heat Shock Factor 1, Heat Shock Protein 70, and 90 Genes in Different Tissues of Air‐Breathing Stinging Catfish ( <scp> <i>Heteropneustes fossilis</i> </scp> )

Air-breathing stinging catfish (Heteropneustes fossilis) often face the problem of exposure to toxic high external ammonia (HEA). The major objectives of the present study were to examine whether HEA exposure causes oxidative stress along with the induction of the heat shock factor (HSF)/heat shock protein (HSP) machinery in stinging catfish. HEA exposure resulted in oxidative stress, as evidenced by a marked rise in hydrogen peroxide (H₂O₂) and malondialdehyde (MDA) levels at the early stage and in GSH levels at the later stage, across multiple tissues. HEA exposure also led to an induction of HSF1 protein and HSC70, HSP70, HSP90a, and HSP90b protein chaperones, as a consequence of upregulation of the corresponding genes in multiple tissues. Immunocytochemical analyses also confirmed the elevated expression of HSF1 and HSP proteins in multiple tissues of the stinging catfish. The marked rise in HSP abundance emphasizes a strong and tissue-specific protective mechanism that reduces cellular impairment from ammonia-induced oxidative stress and associated possible cellular damage, including protein misfolding in stinging catfish. This defense mechanism serves as a fundamental adaptive strategy that allows this air-breathing stinging catfish to survive in the highly toxic environment of ammonia. Collectively, the results demonstrate that HEA acts as a potent environmental stressor, triggering robust activation of the HSF1/HSP axis in H. fossilis. The induction of the heat shock machinery highlights a critical cytoprotective strategy that contributes to the remarkable ammonia tolerance in this air-breathing teleost. These findings enhance our understanding of the molecular defense mechanisms enabling survival in ammonia-rich habitats.