Coordinated response of goldfish antioxidant defenses to environmental stress

Different kinds of oxidative stress cause responses of antioxidant defenses which often act in concert. In previous works, some relationships have been found between oxidative stress markers and antioxidant enzyme activities in goldfish treated with different levels of oxygen or heat shock. This study aimed to check whether or not there are general patterns of relationships between antioxidant enzyme activities and oxidative stress indices in goldfish tissues, regardless of the stressor. For this, goldfish were treated with different concentrations of iron sulphate, 20 or 500 μM, as well as limestone water for 7 days. Both iron ions and limestone water led to a pH shift. Therefore, complex effects of iron ions and/or a pH shift on levels of oxidative stress indices and antioxidant enzyme activities in goldfish liver and kidney were investigated. Experimental conditions resulted in increased protein carbonyl content by 1.5-1.9-fold. Externally added iron ions did not change lipid peroxide levels in the liver but decreased them in the kidney, while levels of thiobarbituric acid reactive substances (TBARS) were elevated by 1.4-2.5-fold. Limestone water raised levels of both lipid peroxidation products in the liver. The treatment affected activities of superoxide dismutase and catalase only slightly, but activities of glutathione-associated enzymes, glutathione-S-transferase (GST), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G6PDH) were lowered in many cases. G6PDH activities correlated inversely with protein carbonyl levels (R2 = 0.77-0.97), suggesting possible inactivation of the enzymes due to their carbonylation. Levels of lipid peroxidation products had a positive correlation to activities of catalase in the liver and GR in the kidney (R2 = 0.83), indicating possible up-regulation of the enzymes by these products. A negative link between TBARS levels and GST activities may reflect the involvement of GST in the detoxification of lipid peroxide products. The main conclusions are: (i) experimental conditions resulted in increased levels of protein carbonyls and end products of lipid peroxidation (TBARS); (ii) under oxidative stress, some enzymes can be inactivated due to oxidation; (iii) lipid peroxidation products seem to be involved in up-regulation of some antioxidant enzymes.