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Fumonisin B1 is a common secondary metabolite produced by Fusarium moniliforme that occurs in corn and corn-based foods. This mycotoxin is toxic to many species of laboratory and domestic animals and is known to induce a variety of diseases such as hepatic cancer and renal and hepatic dysfunction. The structure of fumonisin B1 (FB1) resembles sphingolipids so it can inhibit synthesis of ceramide, an enzyme in the sphingolipid biosynthetic pathway. This inhibition leads to the disruption of sphingolipid metabolism and increased levels of sphinganine and sphingosine (sphingoid bases) in the serum of treated animals. It is believed that the toxicity effect of fumonisin B1 is the result of these sphingoid bases. In the present research, mice were treated with FB1 to determine its pathological effects on gastric gland and gastric mucosa in the treated mice. For this purpose, the mice were randomly assigned into two groups, namely, control ( n = 14) and treatment ( n = 15). The treatment group was fed with prepared food containing FB1 (150 mg/kg) for a period of 4 months. One day after the last treatment, all animals in both groups were euthanized and their stomach were sampled and prepared for microscopic analysis. Histopathological analysis revealed a significant decrease in parietal cell number and a significant increase in the number of inflammatory cells in gastric mucosa. Also, atrophy of gastric glands was observed. The study confirmed that FB1 poisoning can have toxicopathological effects such as gastric gland atrophy and gastritis on mice gastric tissue. [ABSTRACT FROM AUTHOR]

Chlorpyrifos, an organophosphate insecticide, inhibits the enzyme acetylcholinesterse resulting in the accumulation of acetylcholine at the nerve endings. In the present research chlorpyrifos was administered via dermal contact to New Zealand white rabbits to determine its effects on biochemical indices on the rabbits as well as the pathological changes in their liver and brain. Twelve adult male rabbits were randomly assigned to two equal groups ( N = 6; treatment and control group). The treatment group received chlorpyrifos via dermal contact at the doses of 50 mg per kilogram body weight everyday during the first week. The daily doses for the second, third, and fourth weeks were 100, 250, and 400 mg/kg body weight, respectively. The control group received ethyl alcohol as the solvent of chlorpyrifos during the same period. Blood samples from marginal ear vein of both groups were collected on days 0, 7, 14, 21, and 28. Statistical study revealed that chlorpyrifos has harmful effects on the biochemical indices of the treated rabbits. These changes included significant increase in the level of ALP, AST, ALT, and cholesterol in the serum ( p < 0.05, p < 0.01). Also significant decrease was observed in triglyceride and total protein level of the serum in the treatment group as compared with the control group ( p < 0.05). On day 28, the rabbits in both groups were euthanized. Histopathological changes including necrosis of hepatocytes, infiltration of lymphocyte cells, hyperemia, and proliferation of fibroblasts were observed in liver tissue of the exposed rabbits. In addition, necrosis of neuron, encephalitis (perivascular cuffing), hyperemia in blood vessels, gliosis, and necrosis of Purkinje cells in cerebellum were seen in the brain sections. The study confirmed that organophosphate intoxication from chlorpyrifos can occur via dermal exposure. Dermal contact to chlorpyrifos can have toxic effects on biochemical indices. It can also have pathologic effects on the liver and brain tissue. [ABSTRACT FROM AUTHOR]