The aim of this study was to investigate the antioxidant role of zinc (Zn) in the Cd-exposed testes of Wistar rats. Subchronic exposure to Cd (CdCl2, 40 mg/l, per os) for 30 days resulted in a significant reduction in growth rate (-11%) and relative weights of testes (-36%) and seminal vesicles (-80%). Treated rats displayed a decrease in testicular and plasma testosterone levels, respectively (-70%, P<0.05; -48%, P<0.05), epididymal sperm count (-22%, P<0.05), and spermatozoa motility (-35%, P<0.05). In contrast, Cd increased the malondialdehyde (+46%, P<0.05), metallothionein (+200%, P<0.05), and 8-oxodGuo concentrations (+71%, P<0.05) in the testis. In the gonad, Cd decreased the GPx (-30%, P<0.05), CAT (-32%, P<0.05), mitochondrial Mn-SOD (-34%, P<0.05), and cytosolic CuZn-SOD (-32%, P<0.05) activities. Zinc supplementation (ZnCl2, 40 mg/l, per os) in the Cd-exposed rats restored the activities of GPx, CuZn-SOD, and Mn-SOD in the testes to the levels of the control group. Moreover, zinc administration was capable of reducing the elevated levels of malondialdehyde in the testis. Interestingly, zinc supplementation attenuated DNA oxidation induced by Cd in the gonad and restored the testosterone level and sperm count to the levels of the control group. Zinc administration minimized oxidative damage and reversed the impairment of spermatogenesis and testosterone production induced by Cd in the rat testis.

Over recent years, nanotoxicology and the potential effects on human body have grown in significance, the potential influences of nanosized materials on the central nervous system have received more attention. The aim of this study was to determine whether zinc oxide (ZnO) nanoparticles (NPs) exposure cause alterations in emotional behavior and trace elements homeostasis in rat brain. Rats were treated by intraperitoneal injection of ZnO NPs (20–30 nm) at a dose of 25 mg/kg body weight. Sub - acute ZnO NPs treatment induced no significant increase in the zinc content in the homogenate brain. Statistically significant decreases in iron and calcium concentrations were found in rat brain tissue compared to control. However, sodium and potassium contents remained unchanged. Also, there were no significant changes in the body weight and the coefficient of brain. In the present study, the anxiety-related behavior was evaluated using the plus-maze test. ZnO NPs treatment modulates slightly the exploratory behaviors of rats. However, no significant differences were observed in the anxious index between ZnO NP-treated rats and the control group ( p > 0.05). Interestingly, our results demonstrated minimal effects of ZnO NPs on emotional behavior of animals, but there was a possible alteration in trace elements homeostasis in rat brain.

The aim of this study was to assess the potential subacute toxicity of zinc oxide (ZnO) nanoparticles (NPs) in Wistar rats in comparison with reference toxicant, zinc chloride (ZnCl₂), of a non-nanoparticulate form. We therefore studied the relationships between zinc (Zn) accumulation, liver and kidney trace element levels, and plasmatic biochemical parameters. Rats in all groups were treated by intraperitoneal injection of ZnO NPs and/or ZnCl₂ solution (25 mg/kg) every other day for 10 days. The contents of trace element in the liver and kidney were slightly modulated after ZnO NPs and/or ZnCl₂ solution exposure. The same treatment increased the aspartate aminotransferase activity and uric acid concentration. However, ZnO NPs or ZnCl₂ solution decreased the creatinine levels, whereas the combined intake of ZnO NPs and ZnCl₂ decreased the glucose concentration. Interestingly, the analysis of the lyophilized powder of liver using the x-ray diffractometer showed the degradation of ZnO NPs in ZnO-treated group, instead there is a lack of NPs ZnO biosynthesis from the ZnCl₂ solution injected in rats. These investigations suggest that combined injection of ZnO NPs and ZnCl₂ solution has a possible toxic effect in rats. This effect could be related to Zn²⁺ ion release and accumulation of this element in organs. Our findings provide crucial information that ZnO appeared to be absorbed in the organs in an ionic form rather than in a particulate form.

The present study was undertaken to determine the effect of co-exposure to static magnetic field (SMF) and cadmium (Cd) on the antioxidant enzymes activity and DNA integrity in rat brain. Sub-chronic exposure to CdCl (CdCl₂, 40 mg/L, per os) for 30 days resulted in a significant reduction in antioxidant enzyme activity such as the glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD) in frontal cortex and hippocampus. Total GSH were decreased in the frontal cortex of the Cd-exposed group. Cd exposure induced an increase in malondialdehyde (MDA) concentration in the frontal cortex and hippocampus. Moreover, the same exposure increased 8-oxo-7,8-dihydro-2-desoxyguanosine (8-oxodGuo) level in rat brain. Interestingly, the combined effect of SMF (128 mT, 1 hour/day for 30 consecutive days) and CdCl (40 mg/L, per os) decreased the SOD activity and glutathione level in frontal cortex as compared with the Cd group. Moreover, the association between SMF and Cd increased MDA concentration in frontal cortex as compared with Cd-exposed rats. DNA analysis revealed that SMF exposure failed to alter 8-oxodGuo concentration in Cd-exposed rats. Our data showed that Cd exposure altered the antioxidant enzymes activity and induced oxidative DNA lesions in rat brain. The combined effect of SMF and Cd increased oxidative damage in rat brain as compared with Cd-exposed rats.

The aim of this study was to investigate the effect of static magnetic field (SMF) exposure in antioxidant enzyme activity, the labile zinc fraction and DNA damage in THP1 cells (monocyte line). Cell culture flasks were exposed to SMF (250 mT) during 1 h (group 1), 2 h (group 2) and 3 h (group 3). Our results showed that cell viability was slightly lower in SMF-exposed groups compared to a sham exposed group. However, SMF exposure failed to alter malondialdehyde (MDA) concentration (+6%, p>0.05) and glutathione peroxidase (GPx) (-5%, p>0.05), catalase (CAT) (-6%, p>0.05) and superoxide dismutase (SOD) activities (+38%, p>0.05) in group 3 compared to the sham exposed group. DNA analysis by single cell gel electrophoresis (comet assay) revealed that SMF exposure did not exert any DNA damage in groups 1 and 2. However, it induced a low level of DNA single strand breaks in cells of group 3. To further explore the oxidative DNA damage, cellular DNA for group 3 was isolated, hydrolyzed and analysed by HPLC-EC. The level of 8-oxodGuo in this group remained unchanged compared to the sham exposed group (+6.5%, p>0.05). Cells stained with zinc-specific fluorescent probes zinpyr-1 showed a decrease of labile zinc fraction in all groups exposed to SMF. Our data showed that SMF exposure (250 mT, during 3 h) did not cause oxidative stress and DNA damage in THP1 cells. However, SMF could alter the intracellular labile zinc fraction.