The present experiment was designed to access the effects of METHYLMERCURY CHLORIDE (MeHgCl) on antioxidant status, protein concentration, lipid peroxidation and hydroperoxidation in brain parts, spinal cord, lung, heart and pancreas of rats. Twenty male Wistar rats (3 months old) were divided in saline controls (C) and MeHgCl-treated group (MMC). Treated rats were intoxicated with MMC at a dose of 2 mg/kg body weight orally by gavage once a day for 14 consecutive days, for the next 14 days, they were kept intoxicated. Control animals received a corresponding volume of isotonic saline. Health, total feed intake and body weights of rats were monitored daily throughout the study. Both the groups were sacrificed on 29th day. Study revealed an increase in Lipid peroxide (LPO) and Lipid hydroperoxide (LHPO) levels after MeHgCl administration. The levels of superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), total sulfhydryl (TSH) and Protein were significantly declined in all the tissues of MMC treated group as compared to controls. In summary, depletion of antioxidant enzymes in tissues increases MeHgCl accumulation and enhances MeHg-induced oxidative stress, especially LPO and LHPO which plays an important role in tissue degeneration process during MeHgCl intoxication. Results support the hypothesis that depletion of antioxidant enzymes is a primary mechanism of organic mercury toxicity.

Methyl mercury is a well-known environment pollutant toxic to the nervous tissue, particularly during development. At a low concentration Methyl mercury CHLORIDE (MMC) can be transferred to the fetus through the placenta and to newborn offspring through dam. Adult Female wistar rats were inoculated with MMC 0.5, 4.5 and10 mg/kg on the 12th, 13th and 14th gestational days.The newborn offspring were placed with the mother until postnatal day 25. Newborn rats were observed for clinical signs and motor behavior daily. No changes were observed in the clinical signs and motor behavior of these animals.Hippocampus region, CA3 were fixed with 2.5% glutaraldehyde in 0.1 M phosphate buffer and routinely processed embedded in epon 812 and prepared grades were stained with uranyl acetate and lead citrate for electron microscopy study. Results showed several ultrastructural alterations including: chromatin migration to the edge of nuclei, dilation of the smooth endoplasmic reticulum, ribosomes to shed fTom the surface of RER. Mitochondria were rounded with condensed matrical spaces and expanded intercristal spaces and the matrix was condensed.Observation confirms that MMC induces chromatin migration to the edge of nuclei in hippocampus that related to initiation of apoptosis.Furthermore, morphometric analysis confirmed in the cell thickness hippocampus CA3 regions which their mothers received 0.5, 10 mg/kg MMC than control group (p<0.05). So exposure with low doses MMC induced decrease neuronal population in hippocampus CA3 region and may impair memory and learning.

METHYLMERCURY (MeHg) is a well-known environment pollutant toxic to the nervous tissue, particularly during development. At a low concentration METHYLMERCURY CHLORIDE (MMC) can be transferred to the fetus through the placenta and to newborn offspring through breast milk. The purposes of this study were to evaluate ultrastructural alteration in the cerebellum of newborn rat on the 25th postnatal days. Adult Female wistar rats were inoculated with MMC (0.5, 4.5, 10mg/kg /Hg/day) on the 12th, 13th and 14th gestational days. The newborn offspring were placed with the mothers until postnatal day 25. Newborn rats were observed for clinical signs and motor behavior daily. No changes were observed in the clinical signs and motor behavior of these animals. Half of cerebellums were fixed with 2.5% gluteraldehyde in 0.1 M phosphate buffer and routinely processed for electron microscopy and another sample of cerebellum fixed in formalin buffer 10% solution and processing for paraffin section light microscopy and TUNEL assay test.The component cells of the cerebellum male offspring in the 0.5, 4.5, 10 mg /kg groups showed reduction of granular cells layer and apoptosis in neuron cells.ultrastructural study showed chromatin migration to the edge of nuclei, dilation of the smooth endoplasmic reticulum, ribosomes to shed from the surface of RER. Mitochondria were rounded with condensed matrical spaces and expanded intercristal space. And the matrix was condensed.Our observation confirm that MMC induces neuronal injury and apoptosis in cerebellum.

This study carried out in Shahid Marjani farm of Golstan province in autumn 2006. The aim of study was to investigate the effects of organic mercury on beluga (Huso huso) bioenergetics. In practice, four treatment groups of beluga juveniles were exposed to four dietary with MeHg: 1- Control group (0.04 mg/kg) 2- Low dose group (0.76 mg/kg) 3- Medium dose group (7.8 mg/kg) 4- High dose group (16.22 mg/kg) during 70 days. After 42 days, all individuals of high treatment died. There were not significant differences (p>0.05) in Food Consumption Rate (FCR) among the treatment groups. By 35 days the high dose treatment group and by 70 days the medium dose treatment group had significantly depressed growth rate when compared to the control group (p<0.05). The high dose group at 35 days and the medium dose group at 70 days had significantly (p<0.05) lower specific growth rate (SGR) compared all other treatment groups.

Mercury is a unique element that, unlike many metals, has no essential biological function. Wide variety of physiological, reproductive and biochemical abnormalities have been reported in fish exposed, but relatively little is known about METHYLMERCURY (MeHg) bioaccumulation in fishes and how chronic sublethal exposures affect their functioning. Objective of this study was to investigate the assimilation and bioaccumulation of dietary METHYLMERCURY (MeHg) in juvenile Beluga, Huso huso, a commercially important endangered species in the Caspian Sea. In this study four groups of Beluga juveniles were exposed to four dietary treatments with MeHg: 1- Control group (0.04 mg/kg) 2- Low dose group (0.76 mg/kg) 3- Medium dose group (7.8 mg/kg) 4- High dose group (16.22 mg/kg) for a period of 70 days. Results showed that MeHg accumulation was linear during 70 days and in muscle (P<0.05) it was significantly higher in the first 35 days. MeHg bioaccumulation in all treatment groups indicated direct relationship with high dependency between dietary MeHg and MeHg accumulation in muscle (R2=0.0973). Percent assimilation was not significant (P>0.05) among the treatment groups during first and second 35 days, but was higher than second 35 days. It was 57-67% during first 35 days and 42-45% during second 35 days. The results suggested that Mercury contamination could have harmful effects on Beluga even in early years as no exit or transportation for the pollutants exists in the Caspian Sea. The pollutants entering the Caspian Sea through the rivers accumulate in the environment, and a higher amount of them would penetrate into the fish body.