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Biomedical subjects

M Chatterjee

Publications and source records attributed to M Chatterjee.

At least 109 records · Page 6Linked to original sources
PubMed1995

Physiological potential of beta-carotene in prolonging the survival of the host bearing transplantable murine lymphoma.

beta-Carotene, when supplemented in diet, has been found to increase the survival period of mice bearing a transplantable tumor, Dalton's lymphoma. Tumor cell-count, body weight pattern, hematological parameters like total count showed marked alterations in a dose-responsive manner with beta-carotene administration when compared to their untreated counterparts. Decreased tumor cell proliferation is also reflected by increased hemoglobin levels of the host.

Animals↗
PubMed1995

Effects of human placental extract on brain monoamines and monoamine oxidase activity in rats.

Human placental extract, an agent clinically used world-wide in a number of physiological anomalies, has been claimed to be effective in children of slow learners. Since the monoaminergic neurotransmitter systems in the brain play an important role in the processes of learning and memory, we examined the effects of human placental extract on the levels of norepinephrine, dopamine and serotonine in rat brain as an attempt to evaluate the possible underlying biochemical mechanism of action of the extract. We also determined the changes of brain monoamine oxidase (MAO) activity following placental extract treatment. The results showed that subchronic (5, 10, 15 or 20) administration of placental extract (2-4 ml/kg/day) had the effect of increasing all the monoamines and decreasing the MAO activity which could be the possible mode of action of the extract in slow learners.

Animals↗
PubMed1995

Recent kala-azar cases in India: isozyme profiles of Leishmania parasites.

In this study, three WHO recommended reference strains of Leishmania donovani (DD8), L. tropica (K27) and L. major (5 ASKH) were compared by isozyme analysis of 9 soluble enzymes using cellulose acetate electrophoresis (CAE). The isozyme profile of the three species showed distinct electrophoretic mobilities of the enzymes studied. This technique was applied to study the enzyme patterns of 8 clinical isolates of visceral leishmaniasis (VL) and two post kala-azar dermal leishmaniasis (PKDL) collected from the present epidemic (1990s to date). They were seen to be similar to the two isolates of the 1970s epidemic. Interspecies differences were observed in different reference Leishmania species whereas no intraspecies difference was observed amongst the clinical isolates (8VL + 2PKDL) and all of these were found to be similar to L. donovani isolates of 1970s epidemic.

Animals↗
PubMed1995

Beta-carotene prevents lipid peroxidation and red blood cell membrane protein damage in experimental hepatocarcinogenesis.

The anti-cancer efficacy of dietary beta-carotene (BC, 120 mg/kg diet, daily) was evaluated during diethylnitrosamine (DEN, 200 mg/kg body weight)-induced hepatocarcinogenesis in male Sprague-Dawley rats. BC treatment was carried out throughout the study, before initiation or selection/promotion phase of hepatocarcinogenesis in a defined experimental protocol. In red blood cells (RBC) and microsomal fractions from hepatic nodular and non-nodular surrounding parenchyma, the enzymatic lipid peroxidation increased significantly by more than 3-fold, 9- to 10-fold and 4- to 7-fold respectively 18 weeks following initiation by DEN as compared to normal control animals. RBC membrane protein damage was estimated by alanine release and was found to increase more than 5-fold in the same time period in DEN control rats. A decrease in hepatic cytosolic and microsomal glucose-6-phosphatase activities was observed, whereas the activities of the oxygen-derived free-radical scavenger enzymes, like cytosolic catalase and superoxide dismutase, were shown to increase significantly at the same time point. However, BC exposure in the different phases to hepatocarcinogenesis substantially changed all the above parameters in limiting the action of DEN. Results showed that the most significant beneficial effect of BC during hepatocarcinogenesis was exerted mainly in long term continuous and/or the initiation phase of carcinogenicity, rather than in the selection/promotion phase. Moreover, the volumetric and numerical densities of the preneoplastic lesions were all appreciably reduced by exposure to BC. We conclude that long term intake of BC could reduce cancer risk by preventing hepatic lipid peroxidation and RBC membrane protein damage due to its antioxidant actions.

Animals↗
PubMed1994

Anticarcinogenic biological response of Mikania cordata: reflections in hepatic biotransformation systems.

The chemopreventive role of an Indian medicinal plant Mikania cordata (Compositae), which is consumed as vegetable and advocated in folk-medicine, has been evaluated through its effects on Phase 1 and 2 of the hepatic drug-detoxifying enzyme system in rats. Although oral administration of a methanolic extract of this plant root (50, 100 or 150 mg/kg for 4, 8 or 12 weeks) has been found to have very little or no effect on hepatic microsomal cytochrome P-450 and cytochrome b5 contents as well as NADPH cytochrome c reductase activity, it afforded a marked induction of uridine diphosphoglucuronyl transferase activities of liver microsomes. The extract also significantly increased the activities of microsomal uridine diphosphoglucose dehydrogenase, reduced nicotinamide adenine dinucleotide (phosphate): quinine reductase and cytosolic glutathione s-transferases with a concomittant elevation in the contents of reduced glutathione. All these effects were found to be dose-dependent and maintained during 12 weeks of the extract treatment. Results of the study clearly indicate that the intracellular contents of active intermediates of various xenobiotics including chemical carcinogens would be reduced by the specific enhancement of drug-detoxifying enzymes in the liver of rats treated with the plant extract.

Animals↗
PubMed1994

Regulation of eIF-2 alpha-subunit phosphorylation in reticulocyte lysate.

An eIF-2 associated 67-kDa protein (p67) protects eIF-2 alpha-subunit from eIF-2 kinase(s) catalyzed phosphorylation and promotes protein synthesis in the presence of active eIF-2 kinase(s). p67 is a glycoprotein and contains multiple O-linked GlcNAc moieties. We have now studied the roles of hemin, p67, and the glycosyl residues on p67 in the regulation of eIF-2 alpha-subunit phosphorylation in reticulocyte lysates. The results are as follows: (i) Both hemin and p67 inhibited HRI (heme-regulated protein synthesis inhibitor) and dsI (double-stranded RNA activated protein synthesis inhibitor) catalyzed phosphorylation of eIF-2 alpha-subunit in vitro. However, only hemin, and not p67, inhibited casein kinase catalyzed phosphorylation of eIF-2 beta-subunit. (ii) Only p67, and not hemin, inhibited eIF-2 alpha-subunit phosphorylation by eIF-2 kinase(s) in reticulocyte lysate. Significant eIF-2 alpha-subunit phosphorylation was observed even in the presence of hemin when p67 in the reticulocyte lysate was removed by treatment with p67 antibodies. (iii) Reticulocyte lysate contains a p67-deglycosylase in latent form, and hemin prevents activation of this deglycosylase. In the absence of hemin, this p67-deglycosylase is activated. Once activated in the absence of hemin, the activated deglycosylase deglycosylates p67, even in the presence of hemin. This inactivates p67 and allows eIF-2 kinase to phosphorylate eIF-2 alpha-subunit and inhibit protein synthesis. Protein synthesis in reticulocyte lysate is thus regulated by two novel cascades of covalent modifications: protein deglycosylation leading to protein phosphorylation.

Acetylglucosaminidase↗
PubMed1994

Lipid peroxidation, glutathione levels and changes in glutathione-related enzyme activities in streptozotocin-induced diabetic rats.

Levels of lipid peroxidation in liver, kidney, brain and blood, liver glutathione (GSH) and several enzymes in liver tissue associated with antioxidant defence mechanism, namely Catalase (EC: 1.11.1.6), GSH reductase (EC:1.6.4.2) and GSH-S-transferase (EC: 2.5.1.18), were investigated in streptozotocin-induced diabetic rats. The single intraperitoneal injection of streptozotocin (65 mg/kg) caused a four-, eight- and seven-fold increase in lipid peroxidation in brain, liver and kidney, respectively. A decline in GSH levels both in blood (two-fold) and liver (16%) compared with normal counterparts was also observed. A marginal increase in catalase activity, a 20% decrease in GSH reductase and an increase of GSH-S-transferase activity was also found in this experimental diabetic condition. These results suggest experimental diabetes, induced by streptozotocin, can produce biochemical changes not only in pancreas but also in liver, kidney and brain tissue.

Animals↗
PubMed1994

Protective effects of Mikania cordata root extract against physical and chemical factors-induced gastric erosions in experimental animals.

The effect of the methanolic fraction of Mikania cordata (Burm., B. L. Robinson) root extract was investigated for its possible ulceroprotective activity in male Sprague-Dawley rats. Oral administration of this extract (50, 100, or 150 mg/kg) significantly prevented the occurrence of water immersion stress-induced gastric ulcers in a dose-responsive manner. The extract also dose-dependently inhibited gastric ulcers induced by ethanol, aspirin, and phenylbutazone. The ED50 values of the extract in the above four ulcer models were found to be 95.1, 109.7, 125.5, and 136.2 mg/kg, respectively. The volume, acidity, and peptic activity of the gastric juice in pylorous-ligated rats were not altered upon administration of the extract (100 or 150 mg/kg) but it significantly and dose-dependently promoted the gastric mucus secretion in normal as well as stress- and ethanol-induced ulcerated animals. Based on these results, we conclude that M. cordata root extract possesses antiulcer activity and that the observed activity may be due to the modulation of defensive factors through an improvement of gastric cytoprotection.

Animals↗
PubMed1994

Inhibitory effect of beta-carotene on chronic 2-acetylaminofluorene induced hepatocarcinogenesis in rat: reflection in hepatic drug metabolism.

The dietary administration of beta-carotene (BC; 100 mg/kg food) daily has been found to be highly effective in reducing cancer incidence in male Sprague-Dawley rats fed 2-acetyl-aminofluorene (0.05% in food). BC treatment either before initiation, during initiation and selection/promotion phases of hepatocarcinogenesis have been found to be effective in elevating hepatic microsomal cytochrome b5 (24-50%), P-450 (18-38.5%), NADPH cytochrome c reductase (17.5-43.25%) and cytosolic aryl hydrocarbon hydroxylase (60.5-63.5%) activity to a statistically significant level measured either in the hyperplastic nodule (HN) or in the non nodular surrounding liver parenchyma (NNSP) compared to carcinogen control. Moreover, BC treatment throughout the study decrease the cytosolic 1-chloro-2,4-dinitrobenzene conjugated glutathione S-transferase (38.9-51.22%) and microsomal UDP-glucuronyl transferase (37.3-59.1%) activities to a significant level when compared to carcinogen control rats. A decrease in the number of hyperplastic nodules and their total liver parenchyma occupied were also observed in BC treated groups. Furthermore, a direct correlation between HNs and NNSP liver areas were observed with the hepatic BC and vitamin A contents and also with the rates and patterns of hepatic drug metabolism. Our results confirm the fact that BC is particularly protective in limiting the action of 2-AAF during the initiation phase of hepatocarcinogenesis.

2-Acetylaminofluorene↗
PubMed1994

Comparison of acetylcholine-dependent relaxation in large and small arteries of rat mesenteric vascular bed.

The relative contributions of nitric oxide (NO) to in vitro relaxation responses elicited by acetylcholine (ACh) were compared in vessels of different sizes from the rat mesenteric vascular bed. ACh elicited an endothelium-dependent relaxation in phenylephrine-contracted superior mesenteric arteries (SMA, unstretched luminal diam 650 microns), which was blocked by compounds that inhibited NO, such as hemoglobin (10 microM), methylene blue (10 microM), and NG-monomethyl-L-arginine (1 mM). In contrast, the endothelium-dependent relaxation induced by ACh in phenylephrine-contracted mesenteric resistance arteries (MRA, unstretched luminal diam 200 microns) was not blocked by hemoglobin, methylene blue, or NG-monomethyl-L-arginine. KCl (25 mM) partially inhibited the ACh-dependent relaxation in MRA. Furthermore, the ACh-dependent relaxation in MRA was selectively inhibited by the Ca(2+)-activated K+ channel blocker charybdotoxin (0.1 microM). In contrast, the ATP-sensitive K+ channel blocker glibenclamide (50 microM) did not block the ACh-dependent relaxation in MRA. We conclude that 1) NO is a major component of the ACh-dependent relaxation in SMA and 2) the ACh-dependent relaxation of MRA is resistant to NO inhibitors but sensitive to a Ca(2+)-activated K+ channel blocker. This suggests that an endothelium-derived hyperpolarization factor may be involved in the relaxation of MRA.

Acetylcholine↗
PubMed1994

Comparative patterns of hepatic drug metabolizing enzymes and their possible correlation with chromosomal aberrations in transplantable murine lymphoma: a time course study.

The differential levels of induction of hepatic microsomal cytochrome P-450 (cyt. P-450), UDP-glucuronyl transferase (UDPGT), cytosolic glutathione-S-transferase (GSHT) activities, and major chromosomal aberrations were evaluated over various periods of time, following tumor transplantation in male Swiss Albino mice. Changes in the above markers were studied (1) to monitor the entire carcinogenic process and (2) to test the suitability of chemopreventive exposures in terms of phase and duration of tumor growth. The microsomal cyt. P-450 content and the UDPGT activity were significantly elevated (p < 0.01-0.001) from the early stages of tumor growth while the cytosolic GSHT activity reached its highest level (p < 0.01-0.001) only 10 days after tumor transplantation. During the later stages of tumor growth all the biotransforming enzyme activities showed a downhill trend, which was significantly lower than that of their normal counterparts (p < 0.01-0.001). The frequency of different chromosomal aberrations, which were of major structural, numerical, and physiological types, increased steadily throughout the entire length of the carcinogenic process (30 +/- 2 days).

Animals↗
PubMed1994

A novel effect of selenium on streptozotocin-induced diabetic mice.

The effect of oral administration of sodium selenite on glucose homoeostasis was studied in male Swiss albino mice 6 weeks after they were made diabetic with streptozotocin. Diabetes caused hyperglycaemia (2.5-fold), a marked decrease (4.5-fold) in liver glycogen, a 4-fold increase in the glucose-6-phosphatase activity and significant decrease in plasma insulin levels and protein kinase activity. Although selenium administration in control animals showed no significant effect on various parameters measured, selenite treatment of diabetic mice restored these parameters to near control values. Thus the results show insulin-like in vivo action of selenium in diabetic mice.

Animals↗
PubMed1994

Enhanced erythropoietin and suppression of gamma-glutamyl transpeptidase (GGT) activity in murine lymphoma following administration of vanadium.

Administration of vanadium as ammonium monovanadate (0.005 microgram/0.1 ml/mouse/day) was found to reduce the tumor cell proliferation in the host mice bearing Dalton's lymphoma. The high activity of gamma-glutamyl transpeptidase (GGT), a neoplastic marker, was seen in the host cells bearing lymphoma. Vanadium effectively prevented an increase in activity of gamma-glutamyl transpeptidase and maintained a sustained low activity of this enzyme. In addition, an improvement of the hematological aspects of the mice and almost fourfold elevation of erythropoietin (Epo) was obtained following vanadium treatment. This increase in Epo activity may play a vital role in regulating the growth of cellular neoplasia. The present study further confirms the antitumorigenic potential of vanadium in the control of tumor progression in lymphoma via modulating several factors involving erythropoiesis and may emerge as a new chemopreventive agent for the future.

Animals↗
PubMed1994

Mechanism of action of an eukaryotic initiation factor-2 (eIF-2) associated 67 kDa glycoprotein (p67) and an eIF-2 kinase (dsI).

Mechanism of regulation of eIF-2 alpha-subunit phosphorylation by dsI and p67 was studied. The results are as follows: (1) At low dsI concentration, p67 protected equimolar concentration of eIF-2. (2) At high dsI concentration, dsI efficiently phosphorylated eIF-2 alpha-subunit even when equimolar concentrations of both p67 and eIF-2 were present. Significantly increased p67 concentration was necessary to protect eIF-2 alpha-subunit at high dsI concentration. (3) dsI was also phosphorylated as it phosphorylated eIF-2 alpha-subunit. p67 inhibited both eIF-2 alpha-subunit and dsI phosphorylation similarly. (4) Although the [32P]-labelled dsI formed during the reaction could be effectively chased upon subsequent addition of excess unlabelled eIF-2 and ATP, the [32P] labelled eIF-2 formed under identical conditions, retained most of the radioactivity. (5) dsI coimmunoprecipitated with three subunit eIF-2 and p67 inhibited this coimmunoprecipitation reaction. It has been proposed: Three subunit eIF-2 and free p67 are in equilibrium with eIF-2 bound to p67 and, eIF-2.p67 complex is resistant to dsI phosphorylation. Activated dsI is already phosphorylated. At high concentration, dsI(P) can bind to free three subunit eIF-2 and form eIF-2.dsI(P) complex. dsI(P) in this complex then transfers its phosphoryl residue to eIF-2 and forms eIF-2 alpha(P) in an irreversible reaction. In a subsequent reaction, unphosphorylated dsI is autophosphorylated using [gamma 32P]-ATP and the cycle continues. Inhibition of eIF-2 alpha-subunit phosphorylation by p67 blocks this phosphorylation cycle and consequent dsI phosphorylation.

Aminopeptidases↗
PubMed1994

Role of human placental extract on succinic dehydrogenase activity in carrageenin-induced edema in rats in vivo and its effect on erythrocyte lysis, platelet aggregation and trypsin activity in vitro.

Significant increase of liver succinic dehydrogenase (SDH, EC 1.3.99.1) activity was produced by carrageenin-induced edema in rats. Pretreatment with human placental extract inhibited the increased liver SDH activity in a dose-dependent manner. Placental extract was found to have little or no effect on the liver SDH activity in normal rats. Furthermore, heat-induced erythrocyte lysis was inhibited to a substantial extent by the extract and was found to be dose-responsive. However, adenosine diphosphate (ADP)-induced platelet aggregation and trypsin activity were not changed by the placental extract in vitro. The study indicates that the membrane stabilization and depletion of adenosine triphosphate (ATP) synthesis may contribute to antiinflammatory effect of the extract.

Animals↗
PubMed1993

A fluorescence anisotropy study of stabilizing effect of tri- and tetra- nitrovasodilatory drugs on DPPC liposomal membrane.

Glyceryl trinitrate (GT) and pentaerythritol tetranitrate (PT) are two vasodilatory drugs. The physical properties of the membrane lipid matrix, which determine the structure and function of the membrane-bound proteins, generally control the perturbation mechanism of these drugs. Thus, physical interaction of these drugs with membrane lipids is very crucial for their clinical use, different cellular processes, as well as for targetted drug delivery systems. In the present paper, we have reported for the first time the interaction between these drugs and the lipid molecules in the liposomal system of dipalmitoylphosphatidyl-choline (DPPC), as measured by steady-state fluorescence anisotropy using 1,6-diphenyl-1,3,5-hexatriene (DPH) as fluorescent probe. Our results show that by dissolving in the lipid matrix these two drugs effectively stabilise the liposomal membrane: the effect being more in case of GT than in PT, indicating that the rigidifying effect is independent of the number of nitrate groups of the two drugs. This effect increases with the increase in drug concentration, implying solubilisation of all drug molecules. Though our in vitro study has more physical significance than a physiological one, the results obtained here may be used to interpret the effects that are observed in vivo.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1993

Physiological overshoot and the compound action potential.

The sensitivity of the compound action potential (CAP) of the auditory nerve of the Mongolian gerbil (Meriones unguiculatus) to an added signal was studied as a function of the state of adaptation to a masker. The masker consisted of a train of tone bursts. A signal was added to one of the bursts and the threshold for detecting the signal was determined using a two-interval forced-choice technique. With a signal at the same frequency as the masker, there was little or no change in threshold with increasing adaptation to the masker, i.e., with the signal applied at masker onset or later on in the train. With a signal at a different frequency, considerably higher thresholds were obtained in the unadapted state than in the adapted state, a situation that appeared to resemble psychophysical overshoot phenomena. However, the interpretation of this result was complicated by the observation that the CAP response to a two-frequency stimulus is a sum of two slightly desynchronized waveforms arising from different cochlear regions. Synchronizing the two waveforms reduced the 'overshoot', but still resulted in higher thresholds in the unadapted state. The differences in threshold are accounted for by considering the changing signal-to-noise ratios at different states of adaptation. Possible relationships to psychophysically observed overshoot are discussed.

Acoustic Stimulation↗