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Biomedical subjects

A Bhatnagar

Publications and source records attributed to A Bhatnagar.

At least 163 records · Page 9Linked to original sources
PubMed1987

Diethyl pyrocarbonate inactivation of human placental aldehyde reductase II.

Diethyl pyrocarbonate inactivated aldehyde reductase II (L-gulonate:NADP+ 6-oxidoreductase, EC 1.1.1.19) from human placenta. A concentration of 0.5-1.0 mM diethyl pyrocarbonate caused 40-65% loss of activity. The inactivation of the enzyme by diethyl pyrocarbonate was reversed by hydroxylamine and was accompanied by a large change in the absorbance of the protein at 242 nm, but not at 278 nm, indicating that only the histidine residues were modified. NADPH, but not glucuronate afforded significant protection to the enzyme from inactivation by diethyl pyrocarbonate. With 0.2-1.0 mM diethyl pyrocarbonate, 4-5 histidine residues were modified with a pseudo-first-order rate process. A double log plot of the fraction of the unmodified residues indicates that only one functional histidine residue is essential for the catalytic activity of aldehyde reductase II.

Carbohydrate Dehydrogenases↗
PubMed1987

Evidence for the involvement of histidine at the active site of glutathione S-transferase psi from human liver.

The inhibition of catalytic activity of glutathione S-transferase psi (pI 5.5) of human liver by diethylpyrocarbonate (DEPC) has been studied. It is demonstrated that DEPC causes a concentration dependent inactivation of GST psi with a concomitant modification of 1-1.3 histidyl residues/subunit of the enzyme. This inactivation of GST psi could be reversed by treatment with hydroxylamine. Glutathione afforded complete protection to the enzyme from inactivation by DEPC. It is suggested that a functional histidyl residue is essential for the catalytic activity of the enzyme and that this residue is most likely to be present at or near the glutathione binding site (G-site).

Binding Sites↗
PubMed1985

Enzyme immunoassay of serum beta-2-microglobulin levels in various histological forms of leprosy with special reference to its elevation in type I and type II lepra reactions.

The mean beta-2-microglobulin level in serum (3,362 +/- 2,494 micrograms/liter) for 76 leprosy patients, including 9 borderline-tuberculoid, 8 borderline-borderline, 9 borderline-lepromatous, and 16 lepromatous-lepromatous patients and 34 patients with type I or type II lepra reactions, was significantly higher (P less than 0.001) than that (2,122 +/- 1,844 micrograms/liter) for 35 normal subjects. It decreased significantly (P less than 0.001) as the disease glided down from borderline tuberculoid (3,173 +/- 899 micrograms/liter) to the lepromatous end (1,813 +/- 1,391 micrograms/liter). At the onset of type I or type II reaction, the mean beta-2-microglobulin level in serum increased (4,447 +/- 2,863 micrograms/liter), and it remained unchanged (4,433 +/- 2,623 micrograms/liter) after clinical remission. The beta-2-microglobulin level in serum decreased in 55.5% of the patients tested after subsidence of reaction. The level was significantly higher in patients with type II reactions (5,433 +/- 3,299 micrograms/liter) than in patients with type I reactions (3,558 +/- 2,171 micrograms/liter).

Adolescent↗
PubMed1984

Large-bowel malignancy. Epidemiology and gut motility studies in South Asia.

Two hundred thirty-two cases of colorectal malignancy were studied between January 1975 and March 1981. The material was analyzed with respect to various epidemiologic features such as age, sex, residence, religion, socioeconomic status, diet, bowel habits, site of bowel involved, acute obstructive symptoms, and histopathology. The disease afflicted predominantly old people but at an age earlier than is reported in most western studies. Rectal cancer was more common in males, while colonic cancer involved the two sexes equally. Acute large-bowel obstruction was found in 19.4 per cent of patients. The rectum was the most common site (41.8 per cent). Of all the colonic malignancies, 63.4 per cent were in the right colon. Simultaneously, normal gut transit studies using radiopaque markers were conducted in 30 healthy volunteers. The colonic transit rate was 3.09 cm/hour. The markers had a faster gut transit but, interestingly, exhibited pronounced stasis in the right colon, which correlates well with the significantly higher incidence of right-sided malignancy.

Adolescent↗
PubMed1984

Chromosome aberrations and sister-chromatid exchanges (SCEs) in peripheral blood lymphocytes of patients suffering from poliomyelitis.

The frequencies of sister-chromatid exchanges (SCEs) and various chromosome aberrations were studied in blood lymphocyte cultures of individuals suffering from polio virus infection. The frequency of SCEs was found to be within the normal range in polio patients whereas the frequency of chromatid breaks, gaps and other chromosome aberrations showed a significant (p less than 0.001) increase when compared with that of controls. It indicates that the mechanism(s) responsible for polio virus-induced chromosomal damage may not be related to or affect the molecular process(es) that functions in SCE formation.

Cell Transformation, Viral↗
PubMed1983

Role of some radioprotectors on 59Fe uptake in bone marrow after whole-body gamma irradiation to mice.

59Fe uptake in the femur has been studied at four time intervals up to 10 days in mice receiving pretreatment with hydroxytryptophan (HT), AET, MPG and combination of HT and AET or MPG and exposed to 6 Gy whole-body gamma irradiation. MPG or 20 mg/kg dose of AET pretreatment has failed to improve upon the 59Fe uptake depression induced by the gamma irradiation to mice at any of the time intervals. AET (200 mg/kg), HT + AET (20 mg/kg) and HT + MPG treatments though have failed to prevent the initial 59Fe uptake depression induced by the irradiation, have helped a speedy recovery in the iron uptake so that normal level of uptake is obtained on the 7th day. Pretreatment with the HT dose also helps in a speedy recovery as judged on the 7th day and a normal 59Fe uptake is reached in these animals by the 10th day.

5-Hydroxytryptophan↗
PubMedDate not supplied

The effect of oxidants on biomembranes and cellular metabolism.

During the reductive process in the tissues, the aerobes generate a number of oxidants. Unless these oxidants are reduced, oxidative damage and cell death would occur. Oxidation of plasma membrane lipids leads to autocatalytic chain reactions which eventually alter the permeability of the cell. The role of oxidative damage in the pathophysiology of diabetic complications and ischemic reperfusion injury of myocardium, especially the changes in the channel activity which may lead to arrhythmia have been studied. Hyperglycemia activates aldose reductase which could efficiently reduce glucose to sorbitol in the presence of NADPH. Since NADPH is also aldose required by glutathione reductase for reducing oxidants, its diversion would lead to membrane lipid oxidation and permeability changes which are probably responsible for diabetic complications such as cataractogenesis, retinopathy, neuropathy etc. Antioxidants such as butylated hydroxy toluene (BHT) and also reductase inhibitors prevent or delay some of these complications. By using patch-clamp technique in isolated frog myocytes, we have shown that hydroxy radicals generated by ferrous sulfate and ascorbate as well as lipid peroxides such as t-butyl hydroperoxide facilitate the entry of Na+ by oxidizing Na+-channels. Increased intracellular Na+ leads to an increase in Na+/Ca2+ exchange. The increased Na+ concentration by itself may produce electrical disturbance which would result in arrhythmia. Increased Ca2+ may affect proteases and may help in the conversion of xanthine dehydrogenase to xanthine oxidase, consequently increased production of super oxide radicals. Increased membrane lipid peroxidation and other oxygen free-radical associated membrane damage in myocytes has been demonstrated.

Aldehyde Reductase↗
PubMedDate not supplied

Iodine loss from iodised salt on heating.

Iodine deficiency disorders constitute a major public health problem in India. The national IDD control programme (NIDDCP) relies solely on iodine supplementation through fortification of common salt with potassium iodate. However, data regarding iodine loss due to high temperatures of cooking procedure is scarce. Using iodometric titration methods, we calculated iodine content of iodised salt samples subjected to incremental heat up to 350 degree Celsius. The results of the study indicate a gradual but minimal loss of iodine content from the iodised salt samples when subjected to high temperature with a maximum loss noticed being 18.5% at 350 degree Celsius. We conclude that there is minimal loss of iodine from the salt fortified with potassium iodate when subjected to heating (temperature normally attained during cooling process).

Administration, Oral↗