Stress response of aluminium (Al2(SO4)3) toxicity on fish Channa punctatus Bloch has been evaluated via standard stress indicators. The primary stress response in the form of elevated cortisol was evident within 24 hours. The rise of cortisol level was about 170% and it persisted for the next 24 hours. The toxicity also evoked secondary response in the form of increased plasma glucose and C-reactive protein but only after 48 hours of eposure. These stress indicators are very conspicuous and since stress is an energy demanding process hence it is believed that aluminium toxicity has initiated the cortisol release which is responsible for mobilization of glucose from the liver to cope with the stress. The increase in C-reactive protein is an evidence of tissue injuries as a consequence of acute aluminium toxicity.