A characterization of the antioxidant enzyme activity and reproductive toxicity in male rats following sub-chronic exposure to areca nut extracts.

In the present study, areca nut extracts (ANE) administered to male rats by gavage at a dose of 100mg/kg/day for a period of 15, 30, or 45 days resulted in signs of reproductive toxicity. ANE administration resulted in a significant decline (30-57% in epididymal sperm count and 27-61% in sperm motility) as well as substantial abnormalities in sperm morphology. Significant variances in activities of antioxidant enzymes were also observed. Malondialdehyde (MDA) levels, which represent the level of lipid peroxidation, increased by 16-188% and levels of sialic acid decreased by 2-46% compared with that in controls. These results indicate that ANE induced spermatogenic damage, as indicated by a decrease in sperm counts and sperm motility as well as the activity of antioxidant enzymes, an increase in sperm abnormalities, and alterations in sialic acid and MDA levels. Such effects reflect that ANE administration resulted in reactive oxygen species (ROS)-induced oxidative stress in the testis, cauda epididymis, and sperm of male rats.

Effects of acute manganese chloride exposure on lipid peroxidation and alteration of trace metals in rat brain.

Although manganese (Mn) is an essential element, exposure to excessive levels of Mn and its accumulation in the brain can cause neurotoxicity and extrapyramidal syndrome. We have investigated the differences in the accumulated levels of Mn, the degree of lipid peroxidation, and its effects on the levels of trace elements (Fe, Cu, and Zn) in various regions in the brain of rats having undergone acute Mn exposure. The rats in the dose-effect group were injected intraperitoneally (ip) with MnCl2 (25, 50, or 100 mg MnCl2/kg ) once a day for 24 h. The Mn significantly accumulated (p<0.05) in the frontal cortex, corpus callosum, hippocampus, striatum, hypothalamus, medulla, cerebellum, and spinal cord in each case. The rats in the time-course group were ip injected with MnCl2 (50 mg MnCl2/kg) and then monitored 12, 24, 48, and 72 h after exposure. The Mn accumulated in the frontal cortex, corpus callosum, hippocampus, striatum hypothalamus, medulla, cerebellum, and spinal cord after these periods of time, In both the dose-effect and time-course studies, we observed that the concentration of malondialdehyde, an end product of lipid peroxidation, increased significantly in the frontal cortex, hippocampus, striatum, hypothalamus, medulla, and cerebellum. However, no relationship between the concentrations of Mn in the brain and the extent of lipid peroxidation was observed. In addition, we found that there was a significant increase (p<0.05) in the level of Fe in the hippocampus, striatum, hypothalamus, medulla, and cerebellum, but the Cu and Zn levels had not changed significantly. These findings indicated that Mn induces an increase in the iron level, which provides direct evidence for Fe-mediated lipid peroxidation in the rats' brains; these phenomena might play important roles in the mechanisms of Mn-induced neurotoxicology.

Determination of thiobarbituric acid adduct of malondialdehyde using on-line microdialysis coupled with high-performance liquid chromatography.

An on-line analytical system for the continuous monitoring of malondialdehyde (MDA) was developed. This method involves the use of microdialysis perfusion, on-line derivatization and on-line HPLC analysis. This method gave a linear response for MDA concentrations and HPLC peak areas in the range from 0.051 microM to 2.43 microM. The intra-day (RSD = 1.6-10.5%) and inter-day (RSD = 1.1-9.3%) precisions were acceptable. The average in vitro probe recovery of MDA standard was 18.4 +/- 1.0%. The detection limit was 0.03 microM, corresponding to 0.6 pmol for an injection volume of 20 microl. This method was used for in vitro peroxidation investigations, which provided evidence for elevated MDA levels following the incubation of metal ions to a linoleic acid solution.

Brain lipid peroxidation and changes of trace metals in rats following chronic manganese chloride exposure.

The aim of this study was to investigate the effects of chronic, daily, 30-d administration of manganese chloride (MnCl2) to male Sprague-Dawley rats on lipid peroxidation and changes of trace elements (manganese, iron, copper, zinc) in various brain regions. Rats were intraperitoneally injected with MnCl2 (20 mg/kg) once daily for 30 consecutive days. The Mn accumulated in frontal cortex, corpus callosum, hippocampus, striatum, hypothalamus, medulla, cerebellum, and spinal cord. Malondialdehyde, an end product of lipid peroxidation, was markedly decreased in frontal cortex and cerebellum. An increased level of Cu was observed in frontal cortex, medulla, and a cerebellum. A decreased Fe level was found only in cerebellum, and a decreased Zn level was observed in hippocampus and striatum. In a second group of animals, Mn (20 mg/kg/d) and glutathione (GSH, 15 mg/kg/d) were administered ip for 30 d. In CSH-Mn-treated rats, compared to Mn-treated rats, MDA concentrations were significantly reduced in frontal cortex, medulla and cerebellum. The changes of trace elements in rat brain were similar to the Mn-treated group. We suggest that Mn is an atypical antioxidant, as well as not involved in oxidative damage in rat brain. Fe and Cu may play roles in the protective effect of Mn against lipid peroxidation in rat brain.