RESUMO
Despite not being redox-active metals, Cd and Zn can disrupt cellular redox homeostasis by acting pro-oxidatively. The aim of this study was to examine the effects of exposure to Zn (14 and 72 mg/L) and Cd (7.7 and 77 mg/L) for 24 and 48 h on oxidative and antioxidative parameters and the activity of glutathione-S-transferase in Artemia franciscana tissue. In addition, the neurotoxicity of the metals was examined by determining the activity of acetylcholinesterase (AChE). In A. franciscana tissue, Cd (0.0026 ± 0.0001 mg/L) was detected only after 48 h of exposure to 77 mg/L Cd. After 24 h, the 14- and 72-mg/L Zn treatments resulted in significant increases in the Zn concentration (0.54 ± 0.026 mg/L (p < 0.01) and 0.68 ± 0.035 (p < 0.0001), respectively) in A. franciscana tissue compared with the control level, and significant increases were also detected after 48 h (0.59 ± 0.02 (p < 0.0001) and 0.79 ± 0.015 (p < 0.0001), respectively). The malondialdehyde (MDA) concentration in the metal-treated samples was increased after 24 h of exposure, whereas after 48 h, an increase in the MDA concentration was detected only with 7.7. mg/L Cd. A significant increase in the H2O2 concentration after 24 h was measured only after treatment with 72 mg/L Zn. The treatment with 7.7 mg/L Cd for 24 h induced a significant increase in the AChE activity, whereas 48 h of treatment with 77 mg/L Cd and 14 mg/L Zn significantly inhibited AChE. The results indicate that lipid peroxidation resulting from metal toxicity may constitute the basis of neurotoxicity.
