Heavy metals contamination is a serious problem in the aquatic environment. Some of them are very important, having biological roles for aquatic organisms, and called essential heavy metals. In contrast, other heavy metals are considered harmful even at low concentrations. The toxic levels of heavy metals may be of agricultural, industrial and mining activities. This will cause water pollution and changes in the physicochemical characteristics of the aquatic environment. This pollution has deleterious toxic effects on fish and raises concerns over its potential impact on human health. The most common heavy metals are arsenic, chromium, lead and mercury, which affect human health and are considered systemic toxicants. These metals induce organ damage even at low levels of exposure and according to the US Environmental protection agency and international agency for research on cancer, they classified as carcinogens. For all the above reasons, this review was written to contribute to heavy metals' role in the environment, toxic mechanism and toxic effects on fish.
This study was dedicated to detecting the effects of cadmium chloride and of cortisone on experimental infection with Toxoplasma gondii in rats through studying brain tissue. Twenty-four adult albino male rats were used, divided into four groups, comprising: untreated control as group 1, group 2: infected with intraperitoneal injection of Toxoplasma gondii 80 tissue cysts per animal, group 3: infected with Toxoplasma gondii and treated with intraperitoneal injection of cadmium chloride 1.5 mg/kg once a week, group 4: infected with Toxoplasma gondii and treated with intramuscular injection of hydrocortisone in a dose 0.5 mg/kg once a week. After 30 days of treatment for all groups, the animals were sacrificed, and the gross and histopathological examinations were performed on the brains of the rats. The results revealed the presence of changes in the infected groups including appearance of toxoplasma tissue cysts in the grey matter, with mild to moderate perineuronal and periaxonal edema. There were further changes observed in infected groups which treated with cadmium chloride including perineuronal satelletosis, perineuronal edema and demyelination in neuronal axons, otherwise the infected groups treated with cortisone did not show any noticeable difference from the group of infection only. It is concluded that cadmium increase the intensity of occurrence of lesions induced by Toxoplasma gondii in the brain tissue of the rats, considering that all noticeable lesions ranged from mild to moderate in severity, and the differences between groups may be related to the nature of the pathogen used.
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