S C DATTA

A K CHATTERJEE

B B GHOSH

University of Calcutta (informally known as Calcutta University or CU) is a collegiate public state university located in Kolkata, West Bengal, India.&nbsp;Within India it is recognized as a &quot;Five-Star University&quot; and accredited &quot;A&quot; Grade by National Assessment and Accreditation Council.

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The University of Calcutta has secured the Fifth position among the Universities of India in the prestigious &quot;Indian University Ranking 2019&quot; list, released by the NIRF of the Ministry of Human Resource Development, Government of India.

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It was established on 24 January 1857, and was one of the first institutions in Asia to be established as a multidisciplinary and Western-style university. Its alumni and faculty include several heads of state, heads of government, social reformers, prominent artists, only academy award winner and Dirac medal winner in India, many Fellows of the Royal Society and five Nobel laureates as of 2019 which is highest in South Asia.

University Of Calcutta

Journal of Pharmacy and Pharmacology

The effect of deoxypyridoxine on the activities of drug-metabolizing enzymes was investigated in male rats. Phenylbutazone oxidase and aminopyrine N-demethylase decreased in both liver and kidney of deoxypyridoxine-treated rats that received either an 18% or 8% casein diet. However, the magnitude of decrease in activities was more when the rats received an 8% casein diet. The NADPH oxidase activity remained unchanged following deoxypyridoxine treatment. The diminished activities of phenylbutazone oxidase and aminopyrine N-demethylase noted after deoxypyridoxine treatment were restored by pyridoxine supplementation. The decreased activities of drug-metabolizing enzymes in deoxypyridoxine treated rats were not reversed by thyroxine supplementation. It is suggested that pyridoxine in the form of pyridoxal phosphate might be involved in the regulation of drug-metabolizing activities. © 1984, The Japanese Pharmacological Society. All rights reserved.

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The Japanese Journal of Pharmacology

Studies on Certain Drug-Metabolizing Enzymes in Deoxypyridoxine-Treated Rats

Phenylhydrazine administered to rats at a dose of 4mg/100g body weight per day for 3days, diminished the total ascorbic acid level in liver, kidney and spleen tissues. The total ascorbic acid level in blood was, however, elevated after phenylhydrazine treatment. The other effects of phenylhydrazine treatment were a reduction in the activities of D-glucuronoreductase, L-gulonooxidase, dehydroascorbatase and uronolactonase in liver. The dehydroascorbatase activity in kidney was also diminished after phenylhydrazine treatment. The changes in the activities of liver enzymes were found to be accompanied by a diminution in the level of reduced ascorbic acid and an elevation in the dehydroascorbic acid level. It was concluded that the biosynthesis of L-ascorbic acid from both D-glucuronolactone and L-gulonolactone as substrates, was reduced in phenylhydrazine-treated rats. The degradation of L-ascorbic acid by both liver and kidney was diminished by the phenylhydrazine treatment. It was further concluded that phenylhydrazine-treated rats tried to conserve the level of substrate for the synthesis of L-ascorbic acid, by reducing the hydrolytic cleavage of D-glucuronolactone. The elevated blood ascorbic acid level under the same condition was ascribed to the diminished catabolism of L-ascorbic acid. © 1978, Center for Academic Publications Japan. All rights reserved.

Journal of Nutritional Science and Vitaminology

Studies on ascorbic acid metabolism in phenylhydrazine-treated rats.

L-lysine administration to male weanling rats at a dose of 110.4 mg (25% LD50) per 100 g body weight per day for 15 days reduced the liver total ascorbic acid level. The biosynthesis as well as the degradation of L-ascorbic acid was diminished under these conditions. The fall in liver total ascorbic acid level after L-lysine administration was ascribed to its reduced synthesis. © 1977 Birkhäuser Verlag.

Journal	Journal of Pharmacy and Pharmacology
Publisher	-
ISSN	0022-3573