Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.20 (alpha-glucosidase)
 4,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acemannan (ACE-M), a beta-(1,4)-linked acetylated mannan, was evaluated for in vitro activity against human immunodeficiency virus type 1 (HIV-1). Castanospermine (CAS), deoxymannojirimycin (DMN), swainsonine (SWS), azidothymidine (AZT), and dideoxythymidine (DDC) were tested in parallel as control compounds. In vitro antiviral efficacy of ACE-M was evaluated in a variety of cell lines including human peripheral mononuclear, CEM-SS1 and MT-2(2) cells. The virus strain, number of infectious units per cell, and target cell line were important factors in determining the degree of inhibition of viral cytopathic effect in the presence of ACE-M and other control compounds tested. Maximum inhibitory effect was observed in CEM-SS cells infected with the RFII strain of HIV-1. This inhibitory effect was determined to be concentration-dependent. Assay design included primary screening to measure cell viabilities of infected target cells in the presence and absence of test compounds. When tested on HIV-1/RFII-infected CEM-SS cells, the 50% inhibitory effect of CAS (IC50 = 28), an inhibitor of alpha-glucosidase I, was determined to be similar to that observed for ACE-M (IC50 = 45). However, DMN and SWS, inhibitors of mannosidase I and II, tested in parallel to CAS and ACE-M, exhibited no IC50 values. Antiviral potential of ACE-M as an inhibitor of syncytia formation was also explored using CEM-SS cells. Suppression of syncytia formation was observed at an ACE-M concentration of 31.25 micrograms/ml, and complete inhibition was observed at 62.5 micrograms/ml. In addition, HIV-1 RNA levels were studied to establish the antiviral potential of ACE-M in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of AIDS virus replication by acemannan in vitro. 176 65

Sodium diethyldithiocarbamate (DDTC) and sodium N-benzyl-D-glucamine dithiocarbamate (BGD) were compared for their protective effects against cis-diamminedichloroplatinum (DDP)-induced toxicity in kidney and gastrointestinal tract in rats. Rats were injected i.p. with the dithiocarbamates (2.0 mmol kg-1) immediately or 1 h after i.v. injection of DDP (20 mumol kg1). Treatment with BGD immediately or at 1 h after DDP injection effectively prevented the nephrotoxicity of DDP, but administration of DDTC immediately or 1 h after DDP afforded little protection. N-Benzyl-D-glucamine dithiocarbamte significantly reversed the reduction in maltase, sucrase and aminopeptidase activities of jejunal mucosa of rats treated with DDP, whereas treatment with DDTC concurrent with DDP could not reverse the reduction in disaccharidase activity following DDP injection. The platinum concentrations in liver and kidney were significantly decreased by treatment with BGD and DDTC. The treatment with DDTC at 1 h after DDP was more effective on the reduction of platinum concentrations in these tissues than that immediately after DDP. There was no difference between the renal and hepatic concentrations of platinum in two time intervals of BGD. The pharmacokinetic studies indicated that DDTC is more rapidly metabolized than BGD, resulting in larger total clearance and elimination rate constant values. These results reveal that the administration of BGD immediately and at 1 h after DDP can protect against the renal and gastrointestinal toxicities caused by DDP, whereas DDTC afforded little protection, and that the time interval between administration of DDP and DDTC greatly influences its protective effect on DDP-induced toxicity, indicating that the chelation therapy of BGD for DDP is superior to that of DDTC.
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PMID:Comparative effects of diethyldithiocarbamate and N-benzyl-D-glucamine dithiocarbamate on cis-diamminedichloroplatinum-induced toxicity in kidney and gastrointestinal tract in rats. 759 95