Adult males of the Wistar albino rats (Rattus norvegicus) were exposed to lead acetate trihydrate in drinking water (0.0%, 0.25%, 0.5%, 1% and 2% for 1-12 months) to investigate histological and histochemical alterations induced by lead intoxication in the liver. Chronic exposure to subtoxic concentrations of lead produced changes in the hepatocytes, portal triads and the sinusoids. The alterations in the hepatocytes were mainly anisokaryosis, nuclear vesiculation, binucleation, cytoplasmic inclusions, cytoplasmic swelling, hydropic degeneration, necrosis and reduction in glycogen content. In addition, portal triads mild chronic inflammation, Kupffer cells hyperplasia and occasional fatty change were seen together with hemosiderosis. No portal fibrosis or cirrhosis was detected due to chronic subtoxic doses of lead exposure in the liver of any member of the dose groups over the entire period of the study. Chronic lead exposure also increased the activities of alkaline phosphatase and α-glycerophosphate-dehydrogenase which might be an adaptation to the metabolic, structural and functional changes in the organelles of hepatic cells due to lead intoxication. The findings revealed that chronic exposure to lead produced significant histological and histochemical changes in the liver of the Wistar albino rats.

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The present study aimed to investigate the protective role of berberine (BER) against Plasmodium chabaudi-induced infection in mice. Animals were divided into three groups. Group I served as a vehicle control. Group II and group III were infected with 1000 P. chabaudi infected erythrocytes. Group III was gavaged with 100 μl of 10 mg/kg berberine chloride for 10 days. All mice were sacrificed at day 10 post-infection. The percentage of parasitemia was significantly reduced more than 30%, after treatment of mice with BER. Infection caused marked hepatic injuries as indicated by histopathological alterations as evidenced by the presence of hepatic lobular inflammatory cellular infiltrations, dilated sinusoids, vacuolated hepatocytes, increased number of Kupffer cells and the malaria pigment, hemozoin. These changes in livers led to the increased histological score. Also, infection induced a significant increase in liver alanine aminotransferase and aspartate aminotransferase and a significant increase in the total leucocytic count. Moreover, mice became anemic as proved by the significant decrease in erythrocyte number and haemoglobin content. BER showed a significant protective potential by improving the above mentioned parameters. Based on these results, it is concluded that berberine could offer protection against hepatic tissue damage.

Malaria is a major health problem that still affects numerous countries. The current study aimed to identify the role of leaf extract in regulating mouse spleen macrophages during the progression of infection. Three doses of the leaf extract (100, 200, and 300 mg/kg) were administered to mice inoculated with infected erythrocytes. The weight of the infected mice improved after the treatment with. The infection causes disorganization of macrophage distribution in the spleen. After the mice had been treated with the leaf extract, the macrophages appeared to be reorganized in the white and red pulp areas. In addition, the leaf extract (IOLE) significantly increased the total antioxidant capacity of the mice spleens infected with. The phagocytic activity of spleen macrophages was increased in the infected group as indicated by the significant decrease in the number of fluorescent particles in the spleen sections. This number increased in the mice spleens after treatment with IOLE. Based on these results, it is suggested that IOLE regulate macrophage response of the spleen during the blood stage of malaria in mice.

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