Remediation of hypoxia induced brain alteration with pyrimidine treatment in the freshwater catfish, Heteropneustes fossilis.

Low dissolved oxygen (DO), or hypoxia, has a profound impact on the physiological and neurological health of aquatic organisms, particularly oxygen-sensitive organs such as the brain. The aim was to investigate the effects of pyrimidine and its derivative, arylvinylpyrimidine (AVP), on neuronal health in the brain of the lesser studied Heteropneustes fossilis under hypoxic conditions. Laboratory-acclimatized fish were exposed to critical threshold hypoxia (2 mg/L DO for 8 h) based on behavioural and brain histopathology observations. For remediation by pyrimidine and AVP in the hypoxic brain, fish were divided into eight experimental groups; four groups maintained for five days as control [without treatment, with 8 h hypoxia, and only drug effect (pyrimidine, 10 pg/mL or AVP, 0.1 µg/mL)] and four groups were maintained as pre- (drug for five days followed by hypoxia for 8 h) and post- (8 h hypoxia followed by drug for five days) treatment with pyrimidine (10 pg/mL) and AVP (0.1 µg/mL) separately. The results showed that air breather H. fossilis exhibited severe hypoxic effects on neuronal health. Hypoxia significantly elevated antioxidant enzyme activity, and lipid peroxidation (LPO), reduced carbohydrate concentration, and increased total lipid content without affecting total protein level in the brain. The hypoxic brain showed a clear stress effect on cellular and neuronal texture. Hypoxia also significantly influenced neurotransmitter synthesis enzymes [acetylcholinesterase (AChE), tyrosine hydroxylase (TH), dopamine-β-hydroxylase (DBH), and tryptophan hydroxylase-2 (TPH2)]. Hypoxia induced brain alteration was effectively reversed by pyrimidine and AVP treatment. Among different experimental sets, post-treatment being more effective than pre-treatment, and AVP showed greater effectiveness than pyrimidine. These findings demonstrate pyrimidine and AVP as neuroprotective agents against hypoxia-induced damage in the H. fossilis brain and suggest their potential therapeutic utility in managing hypoxia induced neuronal damage in aquatic animals.