Consumption of mercury-contaminated rice induces oxidative stress and free radical aggravation in rats.

OBJECTIVE: To study the oxidative stress induced by consumption of mercury-contaminated rice in rats, and to assess the possible public health risk of mercury contamination in Wanshan mining area. METHODS: Sprague Dawley rats were fed the mercury-contaminated rice produced from Wanshan area for 90 days. The antioxidant status and the free radicals in rat serum were evaluated. RESULTS: High mercury accumulation in organs of rats fed the mercury-contaminated rice confirmed the server pollution of mercury in Wanshan mining area. The intensity of electron spin resonance (ESR) signal increased by 87.38% in rats fed the rice from Wanshan compared with that in the control rats fed the rice from Shanghai, suggesting that chronic dietary consumption of rice from mercury mining area could induce an aggravation of free radicals. Feeding the mercury-contaminated rice was associated with significant decreases in the antioxidant enzymatic activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and concentration of serum nitric oxide (NO), but it had no effect on serum nitric oxide synthase (NOS) activity. Feeding the mercury-contaminated rice raised the level of serum malonyldialdehyde (MDA), indicating the occurrence of oxidative stress. CONCLUSION: The long-term dietary consumption of mercury-contaminated rice induces the aggravation of free radicals and exerts oxidative stress.

[Analyzing the function of different expression genes in the brain of rat exposure to methylmercury using genomics technology].

OBJECTIVE: Analyzing the function of different expression genes in the brain of rat exposure to methylmercury. METHODS: The experimental group of rats were treated with 0.5 mg/kg weight of methylmercury via hypodermic injection. The different expression genes were scanned by using cDNA microarray, and the function genes were analyzed using genomics technology. RESULTS: The gene expression profiles showed that there were 303 genes, in which 170 were upregulated and 133 were downregulated, were differential expressed in the experimental group. Further analysis by bioinformatic technique disclosed that the differentially expressed genes were involved in many biological processes, which included immuno-response and detoxifcation, transfer and expression of genetic information, cell signalling, neurotransduction, cell proliferation and cell differentiation, apoptosis, etc. Cell signaling gene and neurotransduction gene had an very obvious change in the exposure group. CONCLUSION: The signaling pathway was the target by which methylmercury exerted the neurotoxic effects.

[Effect of chronic exposure by mercury contaminated rice on neurotransmitter level changes in rat brain].

In order to survey the potential health risk of environmental exposure by mercury, Sprague-Dawley rats were reared by mercury contaminated rice from mercury mining area. The changes of neurotransmitter acetylcholine (ACh) and acetylcholinesterase (AChE) in rat brain were examined at different times. The results show that the mercury-contaminated rice significantly increase the content of ACh in rat brain after exposure for 7 days. ACh maintained at a high level even after exposure for 30 days, but decreased significantly after exposure for 90 days. The changes of AChE represented an inverse trend compared with that of ACh. The coexisting selenium in rice exhibited antagonistic effects on both mercury accumulation and toxicity. The findings suggested that neurotoxic effects of environmental mercury contamination had been significantly represented after chronically dietary exposure. Further studies are needed to examine the relationship between the neurotransmitter level changes and the Alzheimer's Disease (AD).

Neurotransmitter level changes in domestic ducks (Shaoxing duck) growing up in typical mercury contaminated area in China.

The neurotransmitter level changes of ducks exposed 8-month in a mercury-polluted site (Wanshan, China) and a reference site (Shanghai, China) were examined. Chemical analyses showed both higher mercury and selenium concentrations in the organ of Wanshan ducks. An increased content of acetylcholine (ACh) in brain and blood and a decreased activity of acetylcholinesterase (AChE) in blood were observed. Moreover, there was an increasing trend for nitric oxide synthase (NOS) activity and nitric oxide(NO) production in duck brain, but a reduction of NOS activity in duck serum. The possible explanations were due to the interactive effect of selenium accumulation and the sublethal exposure level of mercury in Wanshan area. The present study showed that AChE and NOS were sensitive to mercury contamination of real circumstance, suggesting that these two indexes have the potential to be biomarkers in assessment of health effects by mercury contamination.