Neuroprotective potential of N -acetylcysteine in carbofuran neurotoxicity: A biochemical and histopathological study

The present study was undertaken to evaluate biochemical markers of chronic carbofuran exposure to rats in terms of lipid peroxide and intrasynaptosomal calcium levels and to correlate them with the histopathological changes in brain regions. A significant increase in lipid peroxidation (LPO) in terms of thiobarbituric acid reactive substances (TBARS) was observed in the cerebral cortex (65%) and brain stem (33%) after carbofuran exposure. This was accompanied by a significant increase (87%) in the intracellular free-Ca²⁺ [Ca²⁺]_i levels. N-acetylcysteine (NAC) administration, on the other hand, reversed the carbofuran-induced increase in LPO and [Ca²⁺]_i. Histopathological studies of carbofuran-exposed brain revealed high frequency of pyknotic neurons in the cerebral cortex and microhaemorrhages in the brain stem. NAC supplementation to carbofuran-treated animals resulted in normalisation of the brain architecture as seen by a reduction in the number of pyknotic nuclei in the cerebral cortex. These findings indicate that increased LPO and elevated [Ca²⁺]_i levels are involved in the development of carbofuran neurotoxicity and are eventually responsible for the pathological alterations. The study also demonstrates potential neuroprotective effect of NAC treatment in carbofuran neurotoxicity.     

Effects of nonylphenol on the brain development-associated gene expression profiles of F1 generation rats

To explore the effects of nonylphenol on brain development-associated gene expression profiles of F1 generation rats by means of microarray technique. The mRNA were extracted respectively from the brain of 2-day-old F1 generation rats whose F0 male generation were tested with and without nonylphenol, respectively, then reversely transcribed to cDNA and labeled with cy5 and cy3 fluorescence. Subsequently,the cDNA probes were hybridized to the Mouse40S cDNA microarray and the fluorescent signals of cy5 and cy3 were scanned and analyzed. Sixteen identified genes expressed differently, including 13 down-regulated in which five were related to brain function and development. Nonylphenol can effect the brain function in many ways, mainly disturb metabolism, development and differentiation of neurocyte, and synthesis and release of neurotransmitter.     

Effects of lithium on membrane fluidity and lipid profile in brain membranes of aluminum-treated rats

The effects of lithium (Li) supplementation on lipid profile and fluidity of cerebrum and cerebellum membranes in aluminum (Al)-treated rats were investigated. A significant decrease in the levels of total lipids and cholesterol was observed in both the regions following Al exposure, which however were significantly increased following Li supplementation. Further, glycolipids and gangliosides contents were significantly decreased in cerebrum, but increased in cerebellum following Al treatment. Interestingly, Li supplementation reversed the trends and regulated the levels of glycolipids and gangliosides. Al treatment also elevated conjugated diene formation and phospholipid levels in both cerebrum and cerebellum membranes, which however were decreased upon Li supplementation. The cholesterol/phospholipid ratio however was decreased after Al treatment and Li supplementation was able to enhance the ratio in both cerebrum and cerebellum. Further, Al treatment significantly increased the fluorescence polarization, anisotropy and order parameter, which however were normalized following Li supplementation. The levels of Al were also found to be significantly elevated in cerebrum and cerebellum after Al treatment and normalized in cerebellum following Li treatment. Therefore, the present study shows the potential of Li in regulating the changes produced by Al on membrane composition and fluidity in rat brain.     

Detection of metallothionein in the intestinal mucosa and brain with 109cadmium∗

Metallothionein (MT) has a great capacity of binding metal ions showing an interesting connection with metal toxicology, as a biochemical marker for environmental metal pollution.

To normal male Wistar rats (200±10 g) and other groups with ferropenic anemia, are administered 1 mg Cd/Kg/day, during 6 days, and MT labelled with the administration 2 h before sacrifice of 3 μCi ¹⁰⁹CdCl₂, also through intragastric catheter. The MT concentration in the intestinal mucosa is expressed in μg MT/g fresh tissue, being for control rats 1.4 ± 0.5; for rats administered with 6 doses of Cd 2.5 ± 0.6 (P<0.05); with ferropenic anemia 4.3±0.7 (P<0.001), and for anemic rats treated with 6 doses Cd 12 + 0,3 (P<0.001) μg MT/g fresh tissue respectively. PAGE 15% T, 2% C_Bis show for intestinal mucosa 2 MT peaks and for brain 3 MT peaks. Anemia induce MT accumulation and increases cadmium incorporation, being anemic subjects eligibles to be submitted first to control and detoxication than the rest of the population, and also MT should be studied as biochemical marker of the pollution.     

汞污染地区粮食对大鼠脑组织氧化损伤影响

应用典型汞矿和典型化工厂粮食对大鼠进行暴露,研究了大鼠脑组织中MAD、SOD、GSHPx以及脑汞含量的变化情况。结果表明,与对照组相比,经过7d暴露后,清镇组大鼠及万山组大鼠脑汞蓄积均出现显著性差异(清镇,p<0.05;万山,p<0.01)。生理生化指标结果表明,暴露3d后,清镇组脑组织GSHPx与对照组相比有显著差异(p<0.05);暴露7d后,万山组脑组织GSHPx及MDA与对照组相比有显著性差异(GSHPx,p<0.05;MDA,p<0.01),清镇组脑组织各指标与对照组相比均有显著性的差异(p<0.05),证明经7d暴露后,大鼠脑组织中已产生脂质过氧化损伤。进而表明上述两处典型汞污染地区汞污染极为严重,可能已经通过食物链严重影响到当地公众健康与安全。