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Biomedical subjects

G Padmanaban

Publications and source records attributed to G Padmanaban.

At least 91 records · Page 5Linked to original sources
PubMed1972

The relationship between delta-aminolaevulinate synthetase induction and the concentration of cytochrome P-450 and catalase in rat liver.

The porphyrinogenic drug 2-allyl-2-isopropylacetamide causes the degradation of microsomal cytochrome P-450 and inhibits the synthesis of catalase in rat liver. The inhibition of catalase synthesis follows the induction of delta-aminolaevulinate synthetase and the consequent overproduction of haem. The allylisopropylacetamide-mediated breakdown of cytochrome P-450 is a rapid event and has a reciprocal relationship to the pattern of delta-aminolaevulinate synthetase induction. Breakdown of cytochrome P-450 appears to be one of the conditions leading to the ;derepression' of delta-aminolaevulinate synthetase.

5-Aminolevulinate Synthetase↗
PubMed1972

Delta-aminolaevulinate dehydratase, the regulatory enzyme of the haem-biosynthetic pathway in Neurospora crassa.

The activity of delta-aminolaevulinate dehydratase is very low in the mould Neurospora crassa compared with the activities detected in bacterial and animal systems. The enzyme is inducible in iron-deficient cultures by addition of iron and is repressed by protoporphyrin. The properties of the purified enzyme indicate its allosteric nature and susceptibility to feedback inhibition by coproporphyrinogen III. Neurospora extracts also contain a protein inhibitor of the enzyme and a small-molecule activator, which appears to be associated with the enzyme. The regulatory function of this enzyme in vivo is correlated with the accumulation of delta-aminolaevulinic acid in normal cultures of N. crassa. The decay curve of the iron-induced enzyme in vivo shows a biphasic pattern, with one of the components showing a half-life of 4-5 min.

Adenosine Diphosphate↗
PubMed1972

Effect of hexachlorobenzene on haem synthesis.

Several drugs are known to induce the liver microsomal mixed-function oxidase system when administered in vivo or even in vitro in cell culture. A sequence of events has been suggested in which the drug is visualized to induce delta-aminolaevulinate synthetase, the first and rate-limiting enzyme of the haem-biosynthetic pathway, which is followed by enhanced haem synthesis and cytochrome P-450 content, facilitating the increase in the drug-metabolizing activity of the liver microsomal fraction. The present studies show that the fungicide hexachlorobenzene, when administered to female rats, can lead to enhanced amounts and rate of synthesis of cytochrome P-450 under conditions when the rate of total haem synthesis has not appreciably altered. The subsequent increase in the rate of total haem synthesis as well as the initial increase in amounts of cytochrome P-450 are brought about under conditions when delta-aminolaevulinate synthetase activity remains constant. However, manifestation of porphyria due to prolonged drug administration is accompanied by a twofold increase in delta-aminolaevulinate synthetase activity. The increase in enzyme activity appears to be due to a decreased degradation rate of the enzyme.

5-Aminolevulinate Synthetase↗
PubMed1971

Haem synthesis during mitochondrogenesis in yeast.

The activities of delta-aminolaevulate synthetase and delta-aminolaevulate dehydratase have been assayed in Saccharomyces cerevisiae during glucose repression and de-repression. delta-Aminolaevulate dehydratase increased concomitantly with the increase in oxygen uptake during the de-repression phase caused by the depletion of glucose in the medium. delta-Aminolaevulate synthetase showed an oscillatory behaviour and a spurt in its activity always preceded the increase in oxygen uptake. The activity of both the enzymes was lowered if the cells were incubated with glucose or cycloheximide, but not with chloramphenicol.

Chloramphenicol↗
PubMed1969

The neurotoxicity of beta-N-oxalyl-L-alphabeta-diaminopropionic acid, the neurotoxin from the pulse Lathyrus sativus.

Intraperitoneal administration of beta-N-oxalyl-l-alphabeta-diaminopropionic acid, the neurotoxin from Lathyrus sativus, to 12-day-old rats causes typical convulsions within 10min. There is a striking accumulation of glutamine in the brain, and chronic ammonia toxicity is indicated. There are no changes in the amounts of urea, aspartic acid and glutamic acid in the brain. Adult rats, even when injected with a dose of excess of beta-N-oxalyl-l-alphabeta-diaminopropionic acid, do not develop symptoms, and there are no changes in the amounts of glutamine or ammonia in the brain. A significant concentration of beta-N-oxalyl-l-alphabeta-diaminopropionic acid can be detected in the brain of the young rat but not in that of the adult animal. It is concluded that beta-N-oxalyl-l-alphabeta-diaminopropionic acid interferes with the ammonia-generating or -fixing mechanisms in the brain and leads to chronic ammonia toxicity.

Age Factors↗