In order to investigate the beneficial effects of 0.5 or 1.0 g/kg Korean garlic juice against the embryotoxicity of 20 mg/kg methylmercury chloride (MMC, CH3HgCl), pregnant Fisher 344 rats were simultaneously orally administered on day 7 of gestation. On day 20 of gestation the dams were laparotomized under ether anesthesia, and the fetuses were removed and examined for toxicity of methylmercury. Garlic juice depressed the toxicity in terms of some parameters. In the case of simultaneous treatment with 0.1 g/kg garlic juice and MMC, rates of increase were 17.5% in maternal body weight, 13.2% and 41.9% in fetal and litters' weight respectively, and 37.0% in fetal survival rate. Decreasing rates were 10.0% in maternal death rate, and 6.9% and 31.3% in pre- and post-implantation loss respectively. Decreasing rates of mercury levels in dams were 67.2% in liver, 57.6% in brain, 47.2% in kidney, 42.1% in spleen and 40.9% in blood. As well, decreasing rates of mercury level in fetuses were 54.9% in all body burden, 55.9% in liver, 46.7% in kidney and 37% in brain, respectively. The number of fetal ossification centers were reduced by 23.8% to 58.0% following simultaneous treatment with 1.0 g/kg garlic juice. These findings indicated that garlic juice effectively inhibited the embryotoxicity of methylmercury in pregnant Fischer 344 rats.
Animal ; Body Weight/drug effects ; Embryo/drug effects* ; Embryo Loss/prevention & control ; Embryo Loss/chemically induced ; Female ; Fetal Weight/drug effects ; Garlic* ; Methylmercury Compounds/toxicity* ; Methylmercury Compounds/pharmacokinetics ; Osteogenesis/drug effects ; Pregnancy ; Rats ; Rats, Inbred F344 ; Tissue Distribution

OBJECTIVETo probe into the prelude marker of central nervous system injury in response to methyl mercury chloride (MMC) stimulation and the signal transduction molecular mechanism of injury in rat brain induced by MMC.

METHODSThe expression of c-fos mRNA in brain and the expression of c-FOS protein in cortex, hippocampus and ependyma were observed using reverse transcription polymerase chain reaction (RT-PCR) and immunocytochemical methods. The control group was injected with physiological saline of 0.9%, while the concentrations for the exposure groups were 0.05 and 0.5, 5 mg/kg MMC respectively, and the sampling times points were 20, 60, 240, 1440 min.

RESULTSThe expression of c-FOS protein in cortex and hippocampus increased significantly, the accumulation of mercury in the brain induced by 0.05 mg/Kg MMC for 20 min had no significant difference compared with the control group. The mean value was 0.0044 mg/Kg, while the protein c-FOS expression had significant difference compared with the control group (P < 0.01). More sensitive expression occurred in hippocampus and cortex, but not in ependyma. Conclusion The expression of c-FOS protein in cortex and hippocampus can predict the neurotoxicity of MMC in the early time, and immediately early gene (IEG) c-fos participates in the process of brain injury induced by MMC.

Animals ; Biomarkers ; metabolism ; Brain ; drug effects ; metabolism ; Cerebral Cortex ; drug effects ; metabolism ; Gene Expression Regulation ; drug effects ; Hippocampus ; drug effects ; metabolism ; Methylmercury Compounds ; pharmacokinetics ; toxicity ; Proto-Oncogene Proteins c-fos ; biosynthesis ; genetics ; RNA, Messenger ; metabolism ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo 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.

METHODSSprague 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.

RESULTSHigh 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.

CONCLUSIONThe long-term dietary consumption of mercury-contaminated rice induces the aggravation of free radicals and exerts oxidative stress.

Animals ; Brain ; metabolism ; China ; Environmental Pollutants ; analysis ; pharmacokinetics ; toxicity ; Food Contamination ; analysis ; Free Radicals ; blood ; Glutathione Peroxidase ; blood ; Industrial Waste ; adverse effects ; Kidney ; metabolism ; Liver ; metabolism ; Malondialdehyde ; blood ; Mercury ; analysis ; pharmacokinetics ; toxicity ; Methylmercury Compounds ; analysis ; pharmacokinetics ; toxicity ; Nitric Oxide ; blood ; Nitric Oxide Synthase ; blood ; Oryza ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; blood