Chhitar M Gupta

Prof. Chhitar M Gupta


Research Focus & Metrics

Academic Career Length

59Years (1968-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 October 1977 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
CGChhitar M Gupta
Chhitar M Gupta
RRR Radhakrishnan
R Radhakrishnan
HKH G Khorana
H G Khorana
Current methods for phospholipid synthesis involving acylation of sn-glycero-3-phosphorylcholine, lysolecithins, and related glycerophosphate esters are not satisfactory. With N,N-dimethyl-4-aminopyridine as a catalyst and moderate amounts of fatty acid anhydrides (1.2-1.5 mol equiv per OH group), diacyl or 1,2-mixed diacylphosphatidylcholines, N-protected phosphatidylethanolamines, and phosphatide acids now can be conveniently prepared in high yields (75-90%). New phospholipids containing photoactivable groups, such as trifluorodiazopropionyl, diazirinophenoxy, 2-nitro-4-azidophenoxy, m-azidophenoxy, and alpha, beta-unsaturated keto groups, in the fatty acyl chains have been prepared. These phospholipids are of interest in studies of lipid-lipid and lipid-protein interactions in biological membranes.

1 March 2000 in Advanced Drug Delivery Reviews
Verified
Journal Article
Closed access
AAAjay K Agrawal
Ajay K Agrawal
CGChhitar M Gupta
Chhitar M Gupta

1 January 1995 in Antimicrobial Agents and Chemotherapy
Verified
Journal Article
Closed access
PDF file
MOM Owais
M Owais
GVG C Varshney
G C Varshney
ACA Choudhury
A Choudhury
SCS Chandra
S Chandra
CGChhitar M Gupta
Chhitar M Gupta
The suitability of liposomes as drug carriers in the treatment of drug-resistant rodent malaria was examined after covalently attaching F(ab')2 fragments of a mouse monoclonal antibody (MAb), MAb F10, raised against the host cell membranes isolated from the Plasmodium berghei-infected mouse erythrocytes, to the liposome surface. The antibody-bearing liposomes thus formed specifically recognized the P. berghei-infected mouse erythrocytes under both in vitro and in vivo conditions. No such specific binding of the liposomes with the infected cells was observed when MAb F10 was replaced by another mouse monoclonal antibody, MAb D2. Upon loading with the antimalarial drug chloroquine, the MAb F10-bearing liposomes effectively controlled not only the chloroquine-susceptible but also the chloroquine-resistant P. berghei infections in mice. The chloroquine delivered in these liposomes intravenously at a dosage of 5 mg/kg of body weight per day on days 4 and 6 postinfection completely cured the animals (75 to 90%) of chloroquine-resistant P. berghei infections. These results indicate that selective homing of chloroquine to malaria-infected erythrocytes may help to cure the chloroquine-resistant malarial infections with low doses of chloroquine.

1 March 1994 in Antimicrobial Agents and Chemotherapy
Verified
Journal Article
Open access
PDF file
AAA Agarwal
A Agarwal
HKH Kandpal
H Kandpal
HGH P Gupta
H P Gupta
NSN B Singh
N B Singh
CGChhitar M Gupta
Chhitar M Gupta
The antitubercular activity of rifampin was considerably increased when it was encapsulated in egg phosphatidylcholine liposomes. A further increase in the activity was observed when the macrophage activator tetrapeptide tuftsin was grafted on the surface of the drug-loaded liposomes. Intermittent treatments (twice weekly) with these preparations were significantly more effective than the continuous treatments. Rifampin delivered twice weekly for 2 weeks in tuftsin-bearing liposomes was at least 2,000 times more effective than the free drug in lowering the load of lung bacilli in infected animals. However, pretreatment with drug-free tuftsin-bearing liposomes did not render the pretreated animals resistant to the Mycobacterium tuberculosis infections, neither did it appreciably increase the chemotherapeutic efficacy of the liposomized rifampin. These results clearly demonstrate that liposome targeting to macrophages could considerably increase the antitubercular activity of liposomized drugs such as rifampin. Also, it shows that immunoprophylactic treatment with macrophage activators such as tuftsin does not afford any advantage in treatment of tuberculosis infections, presumably because of inactivation of the primed macrophages by the mycobacterial sulfatides.

1 March 2004 in Molecular and Biochemical Parasitology
Verified
Journal Article
Closed access
ASAmogh A. Sahasrabuddhe
Amogh A. Sahasrabuddhe
VBVirendra K. Bajpai
Virendra K. Bajpai
CGChhitar M Gupta
Chhitar M Gupta

29 May 1981 in Science
Verified
Journal Article
Closed access
PDF file
CGChhitar M Gupta
Chhitar M Gupta
GMG. C. Mishra
G. C. Mishra
The membranes from normal and Plasmodium knowlesi-infected rhesus monkey erythrocytes (90 to 95 percent infected with early ring stage) were analyzed for transbilayer distribution of phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylserine (PS), by means of chemical and enzymatic probes. The external monolayer of the normal red cell membrane contained at least 68 to 72 percent of the total phosphatidylcholine and 15 to 20 percent of the total phosphatidylethanolamine. In the infected cell, the transmembrane phosphatidylcholine distribution appeared to be reversed, with only 20 to 30 percent of it being externally localized, whereas roughly equal amounts of phosphatidylethanolamine were present in the outer and inner surfaces. However, total phosphatidylethanolamine were present in the outer and inner surfaces. However, total phosphatidylserine in both the infected and normal red cells was exclusively internal. Unlike that in the normal intact cell, external phosphatidylethanolamine in the parasitized cell was readily accessible to phospholipase A2. These results indicate that significant changes in molecular architecture of the host cell membrane are the result of parasitization.