Fucoidan alleviates microcystin-LR-induced hepatic, renal, and cardiac oxidative stress and inflammatory injuries in mice

International audienceFucoidans (FUCs) are sulfated polysaccharides that have a wide range of bioactivities. The current study was designed toevaluate the antioxidant potential of FUC against microcystin-LR (MC-LR)-induced toxicity. Five mice groups (n = 8) wereused. Group 1 received saline, Group 2 received oral FUC 100 mg/kg/day for 21 days, Group 3 received i.p. MC-LR 10 μg/kg/day for 14 days, Group 4 received MC-LR plus FUC 50 mg/kg/day, and Group 5 received MC-LR plus FUC 100 mg/kg/day. Thepresent study showed that MC-LR administration was associated with significant increases (p < 0.01) in serum concentrations ofhepatic (aspartate transferase, alanine transferase, and alkaline phosphatase), renal (urea and creatinine), and cardiac (creatinekinase and CK-MB) injury biomarkers, as well as serum lactate dehydrogenase, cholesterol, and pro-inflammatory cytokines(interleukins-1β and 6, and tumor necrosis factor-α), compared with the control group. Further, MC-LR-intoxicated miceexhibited significantly higher (p < 0.01) hepatic, renal, and cardiac tissue levels of malondialdehyde and nitric oxide, as wellas lower tissue levels of reduced glutathione and activities of glutathione peroxidase, superoxide dismutase, and catalase enzymesin comparison with control mice. Treatment by FUC significantly ameliorated all the above-mentioned alterations in a dosedependent manner with frequent restoration of the normal ranges in the FUC 100 mg/kg/day dose group. Moreover, treatment byFUC alone at 100 mg/kg/day was not associated with significant negative alterations in the assessed biochemical parameters,highlighting its safety at this dose. In conclusion, treatment by FUC significantly ameliorated organ injury, induced by MC-LR inmouse hepatic, renal, and cardiac tissues