Effects Of Cadmium On Hepatopancreas Mitochondrial Antioxidant System And Energetic Metabolism In Freshwater Crab Sinopotamon

To investigate the mechanism of antioxidant system and energetic metabolism of cadmium (Cd2+) on freshwater crab Sinopotamon and to provide the necessary scientific basis for the protection of fisheries and environmental monitoring, the authors studied the effects of Cd2+ on the activities of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and the contents of antioxidant glutathione (GSH), lipid peroxidation product malondialdehyde (MDA); the free radical metabolism of mitochondrial respiratory chain including the capabilities of anti-O2·- and inhibit-OH, the contents of H2O2 and NO, the activity of NOS; the activities of respiratory chain enzymes associated with electron transport and energy production, including reduced nicotinamide adenine dinucleotide oxidase (NADH oxidase), succinate dehydrogenase (SDH) and cytochrome c oxidase (COX) at different concentrations of Cd2+(7.25,14.5,29,58 and 116mg/L) and exposure times (24,48,72 and 96h). The results showed that:(1) Low concentrations of Cd2+ could activate the antioxidant enzymes above and increase the content of GSH. SOD in 48h,29mg/L, CAT at 72h, 14.5mg/L, GPX in 48h,7.25mg/L, GSH at 72h,58mg/L rosed to the highest and had significant differences when compared with controls. With the increase of the Cd2+ concentration and the extension of treatment time, the activities or content started to decline. At 96h, the activity of SOD was directly inhibited, and minimized at 58mg/L which had significant difference compared with the control group. This was similar to the change of GPX activity. The CAT activity at 116mg/L in 24,72 and 96h stabilized at normal levels, showing no significant difference compared with the control group, which was similar to the change of GSH content. However, the MDA content increased persistently after the Cd2+ exposure. It had significantly higher levels at 29mg/L during each treating period, and in 96h,116mg/L, the content reached the maximum which had significant difference compared with the control.(2) With the Cd2+ concentration increased or in the same concentration with the time extended, the mitochondrial anti-O2·- and inhibit-OH capabilities showed a decreasing trend. In contrast, H2O2 content increased gradually. And all reached the peak after 96h,116mg/L, which had significant differences compared with controls; Mitochondrial NO content and NOS activity changed in the similar way, that was, low concentration of Cd2+ could induce the content or activity significantly, and in 72h,29mg/L they rosed to the highest, which had notable differences compared with the control groups. With the increase of Cd2+ concentration and duration of treatment, the content or activity started to decline, and attained the maximum in 96h,116mg/L, which had outstanding differences compared with the controls.(3) The NADH oxidase, SDH activities of the crab mitochondria increased and then decreased, the COX activity was directly inhibited with the increasing Cd2+ concentration when the treatmenting time was 48h. The NADH oxidase, SDH activities reached the maximum in the concentration of 14.5mg/L, the NADH oxidase, COX activities attained the minimum in the concentration of 116mg/L, which had significant differences compared with the control groups; When the time was extended to 96h, in addition to the SDH activity was induced at low Cd2+ concentrations and rosed to the peak in 14.5mg/L, the NADH oxidase, COX activities were directly inhibited, and dropped to the lowest levels in 116mg/L, which had significant differences when compared with controls.These conclusions:(1) After the treatment with cadmium, the major antioxidant enzymes, antioxidant and lipid peroxidation product MDA of the crab mitochondria, the contents of various free radicals which form as a result of electronic omission and NOS activity are affected, indicating that the mitochondrial antioxidant system has been damaged, free radical metabolism disordered. The free radical accumulation will lead to changes in mitochondrial structure and function. (2) The respiratory chain complex activities which are associated with adenosine triphosphate (ATP) formation are also inhibited after cadmium exposure, and such influences are markedly time- and concentration-dependent. It could be speculated that the process of mitochondrial electron transport and oxidative phosphorylation are hindered, energy production disruption is bound to cause tissue damage as for energy shortage.(3) As a target of heavy metal toxicity the indicators of crab mitochondrial antioxidant system and energetic metabolism which are sensitive to change show that the mitochondria physiological and biochemical properties have been affected by cadmium. Therefore, the indicators obtained from experiment could be considered as biomarkers of the heavy metal pollution in aquatic ecosystems for early diagnosis.