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Biomedical subjects

S Banerjee

Publications and source records attributed to S Banerjee.

At least 595 records · Page 33Linked to original sources
PubMed1978

Inhibition of rat liver mitochondrial monoamine oxidase by chloramphenicol and 2-amino-1-p-nitrophenylpropane-1,3-diol.

Inhibition of rat liver mitochondrial monoamine oxidase by chloramphenicol and its hydrolytic product, 2-amino-1-p-nitrophenylpropane-1,3-diol, was studied. The enzyme activity and its inhibition by these two compounds were optimum at pH 7.0 after preincubation for 60 min, the time needed for maximum enzyme--inhibitor complex formation. Enzyme activity could be restored after prolonged dialysis. Monamine oxidase inhibition by chloramphenicol and its hydrolytic product was noncompetitive and reversible. Deamination of various monamines was not to the same degree by these compounds. Of the different antimicrobials studied, only chloramphenicol and its hydrolytic produced has a strong inhibitory effect on monoamine oxidase.

Animals↗
PubMed1978

Long-term effects of partial limb amputation in man.

Ten patients with amputation of part of one arm have been studied electrophysiologically. In each patient the ulnar nerve was stimulated electrically in the amputation stump and at a corresponding level in the intact limb. Control observations were also made on 15 normal subject. In the partially-amputated (PA) limbs the amplitudes of the centripetal ulnar nerve compound action potentials, after maximal stimulation of fast-conducting fibres, were markedly reduced in comparison with the results in control limbs. A small decrease in the mean impulse conduction velocity was observed in the population of PA limbs. In comparison with control observations, stimulation of the ulnar nerve in a PA limb evoked responses in the contralateral somatosensory cortex which were significantly diminished. Simulation of PA limbs caused reflex excitation and inhibition of triceps motoneurones similar to that observed in control subjects. In the intact limbs of the amputees, however, inhibition was reduced, possibly as a consequence of overuse. It is concluded that the receipt of an input from the periphery is essential for the functional integrity of most motor and sensory nerve axons, and probably for fibres in the dorsal column-medial lemniscus pathway.

Action Potentials↗
PubMed1978

Covalent binding of the carcinogen trichloroethylene to hepatic microsomal proteins and to exogenous DNA in vitro.

Studies were carried out on the in vitro covalent binding of the carcinogen trichloroethylene (TCE) to liver microsomal preparations and to exogenous DNA. The binding of TCE to liver microsomal proteins of male C57BL/6 X C3H/He F1 (hereafter called B6C3F1) hybrid mice, a species and strain susceptible to TCE-induced liver tumorigenesis, was 46% higher than that of [14C]TCE to microsomal proteins from male Osborne-Mendel rats, a species and strain resistant to TCE-induced hepatocellular carcinoma. The in vitro binding of [14C]TCE to liver microsomal proteins was 37% higher for male B6C3F1 mice; female B6C3F1 mice that have been reported to show a lower incidence of TCE-induced hepatocellular carcinoma than do males. Microsomal proteins from the lung, stomach, and kidney of B6C3F1 hybrid mice also metabolized TCE, as indicated by the covalent binding of [14C]TCE to microsomal proteins from these organs. For rats the binding of TCE to liver microsomal proteins of Sprague-Dawley animals was higher than that of Osborne-Mendel and Fischer 344 rats. Incubation of [14C]TCE with salmon sperm DNA in the presence of microsomal preparations from B6C3F1 hybrid mice resulted in covalent binding of [14C]TCE to DNA. This binding was much higher in the presence of microsomal proteins from male rather than female mice. The binding to DNA and protein was enhanced by in vivo phenobarbital administration. The effects of 1,2-epoxy-3,3,3-trichloropropane on the covalent binding of [14C]TCE to protein and DNA were also examined.

Animals↗
PubMed1977

Smooth muscle relaxant properties and vasomotor actions of 2-amino-1-p-nitrophenylpropane-1,3-diol.

Experiments with the guinea pig ileum, trachea, and vas deferens, the rat fundal strip, the rabbit jejunum and aortic strip, and the toad heart indicated that 2-amino-1-p-nitrophenylpropane-1,3-diol, the hydrolytic product of chloramphenicol, inhibited smooth muscles. Its action was direct and not through any mediators. After intravenous administration, the compound produced vasodepression followed by an overshooting rise of blood pressure. Vasodepression was not mediated by adrenergic, cholinergic, or histaminergic mechanisms. Hypertension was a sympathomimetic effect. Muscle relaxant and cardiovascular effects of the compound were similar to those of chloramphenicol, although it had no antibacterial effect.

Animals↗
PubMed1977

Enzymatic responses of transplanted tumour cells towards estrogen, progesterone and testosterone.

The influence of estrogen, progesterone and testosterone on the activities of alkaline and acid phosphatases, adenosine triphosphatase and succinate dehydrogenase were determined by cytochemical methods in sarcoma 180 and Ehrlich's carcinoma cells transplanted in male and female Swiss mice. The results revealed differential effects of the sex hormones on different enzymes which seemed to depend on the type of tumour cell studied and the sex of the host mice.

Acid Phosphatase↗
PubMed1976

Muscle relaxant properties of chloramphenicol.

Experiments with the guinea pig ileum, guinea pig trachea, rat fundal strip, rat colon, rat vas deferens, and toad heart indicated that chloramphenicol inhibited smooth muscles, decreasing both the height and frequency of spontaneous contraction. Chloramphenicol-induced relaxation was not mediated through adrenergic, cholinergic, or histaminergic mechanisms. The degree of muscle relaxation was related to the concentration of chloramphenicol, and the relaxant effect could be reversed by removing chloramphenicol from site of action by washing. Its action appears to be direct on the muscle, possibly by interfering with the energy-generating mechanism.

Animals↗
PubMed1976

Fluorescence studies on the interaction of the tumor promoter phorbol myristate acetate and related compounds with rat liver plasma membranes.

The interaction of the potent tumor-promoting agent phorbol myristate acetate (PMA) with purified rat liver plasma membranes suspended in phosphate-buffered saline (PBS), pH 7.4, was studied by fluorescence spectrophotometry. Exposure of membranes to PMA caused up to 21% decrease of the native membrane emission, i.e. the fluorescence of both tryptophan and tyrosine, compared to non-treated membranes. The decrease in the membrane emission varied with both the PMA and the membrane concentration. Treatment of rat liver plasma membranes with biologically less active analogs of PMA, phorbolol myristate acetate (PHMA) and 4a alpha-phorbol didecanoate (4a alpha-PDD), resulted in a 5-10% decrease of the native membrane emission. These studies suggest that PMA causes alterations in membrane structure which are due, at least in part, to conformational changes in the membrane proteins.

Animals↗
PubMed1976

The transport of tetracyclines across the mouse ileum in vitro: the effect of cations and other agents.

The intestinal transfer of different tetracyclines dissolved in calcium- and magnesium-free Krebs bicarbonate buffer solution, pH 7.4, was studied using the everted ileum of the mouse. The rates of transfer of chlortetracycline and demethylchlortetracycline were less than those of tetracycline and oxytetracycline, the latter compounds being transferred at the same rate. Addition of calcium and magnesium to the buffer greatly reduced the transfer of tetracycline; this inhibition could be antagonized by EDTA. The presence of iron also inhibited the transfer of tetracycline. The inhibitory effect of these ions on tetracycline transfer seemed due to chelation of the drug. Glucosamine and acetylmethionine, but not acetyl glucosamine, diminished the intestinal transfer of tetracyclines. The former two agents did not influence the uptake of tissue fluids. Tetracycline was also transfered from the serous to the mucous coat in the non-everted intestinal sac of mice. The above observations suggested that the absorption of tetracyclines was not due solely to passive diffusion.

Animals↗