Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ammonium chloride at a concentration of 20 mM delayed by 4-5 hr the production of virus progeny in mouse L-2 cells infected at high multiplicity with mouse hepatitis virus (MHV). This delay was seen in the production of both intracellular and extracellular virus. However, the final titers were similar to those produced by MHV-infected cells maintained in normal medium. The manifestation of virus-induced cell fusion was similarly found to be delayed, but not otherwise decreased in severity, when ammonium chloride was present in the culture medium. Ammonium chloride caused similar delays in production of virus-specific, positive-sense RNAs and of viral polypeptides. The relative proportions and apparent molecular weights of viral RNAs and polypeptides were similar to those found in MHV-infected cells cultured in normal medium. In vitro translation of endogenously produced viral RNAs in cell extracts, prepared from MHV-infected cells, was not inhibited by ammonium chloride. Thus, ammonium chloride has no specific, inhibitory effect on viral protein synthesis. Ammonium chloride did not reduce the number of virus-infected cells in culture, as monitored by infectious center assay. Analysis of early events in MHV infection showed that ammonium chloride did not affect adsorption or internalization of MHV by L-2 cells. However, the subsequent eclipse phase, as monitored by decline in infectivity of internalized virus inoculum proceeded less efficiently in the presence of ammonium chloride. On the basis of the known inhibitory effects of ammonium chloride on lysosomal/endosomal functions, the results suggest an endosomal mechanism of MHV uncoating. Thus the primary effect of ammonium chloride on MHV infection of L-2 cells is to attenuate virus uncoating, thereby chronologically displacing all subsequent virus-encoded functions.
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PMID:Attenuation of murine coronavirus infection by ammonium chloride. 299 91

Drug-induced liver injury is the leading cause for more than 50 percent of cases of acute liver failure. This study was conducted on herbo-mineral formulation "Hepcon" to evaluate its hepatoprotective effects in drug induced hepatitis in experimental animals. The liver injury was introduced with over dosage of non steroidal anti-inflammatory drugs (NSAIDs) and carbon tetrachloride (CCl4). The herbo-mineral formulations "Hepcon" consist of Zingiber officinale, Piprum nigrum, Ammonium chloride and Arsenic trioxide (Hartal warqi). The aqueous extraction was administered to experimental animals. Thereafter their LFTs, IgG, and tissue pathology was studied. It was observed on the basis of biochemical and histopathological analysis that animals which were subjected to Hepcon became normal in 60 days whereas those as control group did not showed improvements and most of them died. It was concluded that the efficacy of Hepcon to treat liver injury caused by CCl4 and NSAIDs is very effective, and no side effects were noticed.
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PMID:Efficacy of herbal coded Hepcon on drug induced hepatitis in experimental animals through histopathological and biochemical analysis. 2403 58