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Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. In laboratory animal models, diethylnitrosamine (DENA) is a well-known agent that has a potent hepatocarcinogenic effect that is used to induce HCC. As curcumin has a potent anti-inflammatory effect with strong therapeutic potential against a variety of cancers, our present study aims to investigate its curative effects and the possible mechanisms of action against DENA-induced HCC in male rats. Investigation of biochemical and molecular parameters of HCC animal model liver showed an overexpression of TGF-β and Akt proteins accompanied with a significant reduction of the proapoptotic marker caspase-3. DENA-induced hepatic cellular injury resulted also in a significant increase in liver function marker enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lipid peroxides in this group. Curcumin treatment partially reversed DENA-induced damage as it reduced the overexpression of the angiogenic and anti-apoptotic factors TGF-β and Akt and improved caspase-3 expression. Also, it could partially normalize the serum values of liver marker enzymes and lipid peroxidation and improve liver architecture. Curcumin shows a unique chemotherapeutic effect in reversing DENA-induced HCC in rat model. This effect is possibly mediated through its proapoptotic, antioxidant, anti-angiogenic, as well as antimitotic effects. It interferes and modulates cell signaling pathways and hence turns death signals and apoptosis on within tumor cells.

Liver sinusoids are lined by fenestrated endothelial cells surrounded by perisinusoidal cells, Kupffer cells, and pit cells, as well as large granular lymphocytes. The functional ability of the liver cells can be substantially modified by exposure to toxins. In the current work, we assessed the histopathological and ultrastructural effects of a time-course exposure to aflatoxin B1 (AFB1) on the hepatic structures of rats. A total of 30 adult female Wistar rats were randomly divided into three groups: a control group, a group orally administered 250 µg/kg body weight/day of AFB1 for 5 days/week over 4 weeks, and a group that received the same AFB1 treatment but over 8 weeks. Histopathological and ultrastructural examinations of hepatocytes revealed massive vacuolar degeneration and signs of necrosis. Furthermore, the rat liver of the treated group exhibited damage to the sinusoidal endothelium, invasion of the space of Disse with hyperactive Kupffer cells, and some immune cells, as well as Ito cells overloaded with lipids. In addition, damaged telocytes were observed. Taken together, our results indicate that AFB1 induces irreversible adverse effects on the livers of rats.

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Bisphenol A (BPA) is intensely used in the production of polycarbonate plastics and epoxy resins. Recently, BPA has been receiving increased attention due to its link to various health problems that develop after direct or indirect human exposure. Previous studies have shown the harmful effect of high doses of BPA; however, the effect of small doses of BPA on disease development is controversial. The aim of this study was to investigate the effect of a low dose of BPA on the rat myocardium and to explore the outcome of coadministration of Omega-3 fatty acid (FA). Thirty adult male rats were divided equally into control group, BPA-treated group (1.2 mg/kg/day, intraperitoneally for 3 weeks), and BPA and Omega-3-treated group (received BPA as before plus Omega-3 at a daily dose of 300 mg/kg/day orally) for 3 weeks. Exposure to BPA resulted in structural anomalies in the rat myocardium in the form of disarrangement of myofibers, hypertrophy of myocytes, myocardial fibrosis, and dilatation of intramyocardial arterioles. On the other hand, mast cell density and media-to-lumen area ratio were not significantly altered. Interestingly, concomitant administration of Omega-3 FAs with BPA significantly reduced BPA-induced changes and provided a protective effect to the myocardium. In conclusion, exposure to a low dose of BPA could potentially lead to pathological alterations in the myocardium, which could be prevented by administration of Omega-3 FA.

Introduction: Bisphenol A (BPA), a well-known industrial chemical, has adverse effects on the brain even at relatively low exposure levels in rodents, primates and humans. Omega-3-fatty acids participate in a number of neuronal processes including neurogenesis, neuron differentiation, and neuro-protection. Aim of the work: To investigate the possible protective action of omega-3-fatty acids on the injurious histological effect induced by Bisphenol A on rat hippocampus. Materials and Methods: Eighteen adult male Wistar rats were divided into 3 equal groups; control, BPA (1.2mg/kg daily for 3 weeks, intraperitoneally) and the third group were given omega-3 (300mg/kg orally) in addition to BPA in the aforementioned dose and duration. Hippocampus sections were processed for hematoxylin and eosin staining, GFAB staining and electron microscopic examination. Results: BBPA administration resulted into several histological alterations. Glial fibrillary acidic protein-positive cells were more abundant in the hippocampus of BPA-treated animals compared with the control animals. Ultra-structurally, the hippocampus of BPA-treated group showed nerve cells having nuclei with irregular outline and dilated perinuclear envelop, dilated RER and Golgi, swollen mitochondria with destroyed cristae. Some of the myelinated and unmyelinated nerve fibers showed degenerative changes. Concomitant administration of omega-3-fatty acids ameliorated these effects. Conclusions: OOmega-3-fatty acids partially minimized the severity of BPA-induced hippocampus injurious histological effects in Wistar rat.

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