Bovine herpesvirus-5 infection in a rabbit experimental model: immunohistochemical study of the cellular response in the CNS.

Since little information is available regarding cellular antigen mapping and the involvement of non-neuronal cells in the pathogenesis of bovine herpesvirus type 5 (BHV-5) infection, it were determined the BHV-5 distribution, the astrocytic reactivity, the involvement of lymphocytes and the presence of matrix metalloproteinase (MMP)-9 in the brain of rabbits experimentally infected with BHV-5. Twelve New Zealand rabbits that were seronegative for BHV-5 were used for virus inoculation, and five rabbits were used as mock-infected controls. The rabbits were kept in separate areas and were inoculated intranasally with 500 µl of virus suspension (EVI 88 Brazilian isolate) into each nostril (virus titer, 10(7.5) TCID50). Control rabbits were inoculated with the same volume of minimum essential medium. Five days before virus inoculation, the rabbits were submitted to daily administration of dexamethasone. After virus inoculation, the rabbits were monitored clinically on a daily basis. Seven rabbits showed respiratory symptoms and four animals exhibited neurological symptoms. Tissue sections were collected for histological examination and immunohistochemistry to examine BHV-5 antigens, astrocytes, T and B lymphocytes and MMP-9. By means of immunohistochemical and PCR methods, BHV-5 was detected in the entire brain of the animals which presented with neurological symptoms, especially in the trigeminal ganglion and cerebral cortices. Furthermore, BHV-5 antigens were detected in neurons and/or other non-neural cells. In addition to the neurons, most infiltrating CD3 T lymphocytes observed in these areas were positive for MMP-9 and also for BHV-5 antigen. These infected cells might contribute to the spread of the virus to the rabbit brain along the trigeminal ganglia and olfactory nerve pathways.

Effect of lycopene on nephrotoxicity induced by mercuric chloride in rats.

Oxidative stress is an important molecular mechanism for kidney injury in mercury poisoning. We studied lycopene, a potent carotenoid found in tomatoes due to its large antioxidant properties, and also evaluated the ability of lycopene to prevent HgCl(2) nephrotoxicity. Rats were injected with HgCl(2) (0 or 5 mg/kg body weight, subcutaneously) 6 hr after lycopene administration (0, 10, 25 or 50 mg/kg by gavage) and were killed 12 hr after HgCl(2) exposure. HgCl(2)-induced inhibition of delta-aminolevulinate dehydratase activity (approximately 35%) and increase of lipid peroxidation in kidney (approximately 37%) were prevented by lycopene. However, lycopene did not prevent the increase of plasma creatinine levels (approximately 123%) and renal tubular necrosis induced by HgCl(2). Glutathione peroxidase and catalase activities were enhanced (approximately 71% and approximately 41%), while superoxide dismutase activity was depressed (approximately 44%) in HgCl(2)-treated rats when compared to control and these effects were prevented by lycopene. Our results indicate that although lycopene did not prevent HgCl(2)-induced renal failure, it could play a beneficial role against HgCl(2) toxicity by preventing lipid peroxidation and changes in the activity of delta-aminolevulinate dehydratase and antioxidant enzymes.