Oxidative effects and toxin bioaccumulation after dietary microcystin intoxication in the hepatopancreas of the crab Neohelice (Chasmagnathus) granulata

• We studied the accumulation and depuration of microcystin LR in an estuarine crab.
• We analyzed MCLR effects on the oxidative balance.
• Oxidative damage could be reversed by increased detoxifying mechanisms.

We studied the accumulation and depuration of microcystin-LR (MCLR) in the hepatopancreas of the crab Neohelice granulata fed twice weekly with either non toxic or MCLR-producing Microcystis aeruginosa (strain NPDC1 or NPJB, respectively) during seven weeks. We also analyzed MCLR effects on the oxidative stress- and detoxification-related variables, superoxide dismutase and glutathione-S-transferase activities, and the levels of reduced glutathione and lipid peroxidation (as thiobarbituric acid reactive substances, TBARS).Hepatopancreas MCLR content slightly increased during the first three weeks, up to 8.81±1.84 ng g−1 wet tissue mass (WTM) and then started to decrease to a minimum of 1.57±0.74 ng g−1 WTM at the seventh week (p<0.05 with respect to that in the first week). TBARS levels were about 55% higher in treated than in control N. granulata (p<0.001 and p<0.05) during the first three weeks of the experimental period. GSH content became 50% lower than in control individuals (p<0.01) during weeks 6 and 7. SOD activity was increased by about 2-fold (p<0.05 or p<0.001) from week 3 to 7 in treated crabs with respect to control ones, while GST activity was about 70% higher in treated than in control crabs from week 4 to week 7 (p<0.05).Our data suggest that in the hepatopancreas of N. granulata MCLR accumulation and oxidative damage are limited and reversed by detoxification-excretion and antioxidant mechanisms. The activation of these defensive mechanisms becomes evident at 3-4 weeks after the start of the intoxication.