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Biomedical subjects

M Chatterjee

Publications and source records attributed to M Chatterjee.

At least 73 records · Page 4Linked to original sources
PubMed1997

Effect of thiocyanate ingestion through milk on thyroid hormone homeostasis in women.

A thyroid-hormonal evaluation of thirty-five women consuming commercially packed milk containing thiocyanate was carried out. The mean serum thiocyanate concentration, which was measured by the FeCl3 colour test, was significantly higher (P < 0.01) than that of control subjects. Serum thyroxine (T4), triiodothyronine (T3) and thyroid-stimulating hormone (TSH) concentrations of exposed women were compared with those of thirty-five control subjects. Thiocyanate ingestion was associated with lower levels of T4 (P < 0.01) and higher levels of TSH (P < 0.01) compared with the control subjects. T3 was found to be higher in the women consuming thiocyanate-containing milk but the difference was not significant. The serum T4 level was found to be negatively correlated (r -0.359, P < 0.05) while the TSH level was positively correlated (r 0.354, P < 0.05) with thiocyanate concentration in the exposed group. From this study, it appears that ingestion of milk with added thiocyanate impairs thyroid function.

Animals↗
PubMed1997

Vanadium-mediated chemoprotection against chemical hepatocarcinogenesis in rats: haematological and histological characteristics.

The trace element vanadium was investigated for its anti-neoplastic role in relation to haematological status, hepatic histopathology and histochemical analysis of glycogen in liver. Its impact on the survival of male Sprague-Dawley rats subjected to a two-stage hepatocarcinogenesis regimen was also assessed. Initiation was performed using a single intraperitoneal injection of diethylnitrosamine (DENA) (200 mg/kg) followed by promotion with phenobarbital (0.05%) in a basal diet. Vanadium supplementation as ammonium monovanadate at 0.5 ppm vanadium in drinking water was given ad libitum throughout the experiment (20 weeks), before the initiation (4 weeks), or during the promotional period (14 weeks). At the end of the study, there was a significant decrease in red blood cell count, haemoglobin content, haematocrit value, mean corpuscular haemoglobin, mean corpuscular haemoglobin concentration, plasma volume change and total white cell count, with a concurrent alteration in lymphoid:myeloid ratio in DENA control animals compared with their normal counterparts. Vanadium supplementation throughout the study or before the initiation significantly reversed the DENA-induced alterations in most of the haematological indices. A single intraperitoneal injection of DENA also depleted the plasma albumin concentration, raised the plasma globulin content, and decreased the ratio of albumin to globulin. These altered features began to return to normal following vanadium supplementation. Supplementary vanadium also elicited substantial protection against DENA-mediated rat liver carcinogenesis. This was fairly evident from hepatic histology and evaluation of glycogen accumulation by periodic acid-Schiff reaction. The survival of DENA-treated animals was considerably increased in the presence of vanadium. The critical involvement of vanadium in modulating several factors associated with erythropoiesis under carcinogenic challenge may thus have a possible impact on the eventual increased survival of the host.

Administration, Oral↗
PubMed1997

Binding of a thrombin receptor tethered ligand analogue to human platelet thrombin receptor.

A thrombin receptor-radioligand binding assay was developed using [3H]A(pF-F)R(ChA)(hR)Y-NH2 ([3H]haTRAP), a high affinity thrombin receptor-activating peptide (TRAP), and human platelet membranes. Scatchard analysis of saturation binding data indicated that [3H]haTRAP bound to platelet membranes with a Kd of 15 nM and a Bmax of 5.2 pmol/mg of protein. The binding was reduced by GPPNHP, a nonmetabolizable GTP analogue. Various TRAPs and a TRAP antagonist, but not other receptor agonists, displaced [3H]haTRAP from the binding sites. SFLLRN-NH2, a thrombin receptor-tethered ligand analogue, and [3H]haTRAP exhibited competitive binding for the same binding sites. The relative affinity of these peptides for the binding site paralleled their EC50 or IC50 values for platelet aggregation. These data indicate that [3H]haTRAP binds specifically and saturably to the functioning G protein-linked thrombin (tethered ligand) receptor in human platelet membranes.

Dose-Response Relationship, Drug↗
PubMed1996

From seed germination to flowering, light controls plant development via the pigment phytochrome.

Plant growth and development are regulated by interactions between the environment and endogenous developmental programs. Of the various environmental factors controlling plant development, light plays an especially important role, in photosynthesis, in seasonal and diurnal time sensing, and as a cue for altering developmental pattern. Recently, several laboratories have devised a variety of genetic screens using Arabidopsis thaliana to dissect the signal transduction pathways of the various photoreceptor systems. Genetic analysis demonstrates that light responses are not simply endpoints of linear signal transduction pathways but are the result of the integration of information from a variety of photoreceptors through a complex network of interacting signaling components. These signaling components include the red/far-red light receptors, phytochromes, at least one blue light receptor, and negative regulatory genes (DET, COP, and FUS) that act downstream from the photoreceptors in the nucleus. In addition, a steroid hormone, brassinolide, also plays a role in light-regulated development and gene expression in Arabidopsis. These molecular and genetic data are allowing us to construct models of the mechanisms by which light controls development and gene expression in Arabidopsis. In the future, this knowledge can be used as a framework for understanding how all land plants respond to changes in their environment.

Germination↗
PubMed1996

DAG, a gene required for chloroplast differentiation and palisade development in Antirrhinum majus.

We have identified a mutation at the DAG locus of Antirrhinum majus which blocks the development of chloroplasts to give white leaves with green revertant sectors. The green areas contain normal chloroplasts whereas the white areas have small plastids that resemble proplastids. The cotyledons of dark-grown dag mutant seedlings have plastids which also resemble proplastids. The palisade cells in the white areas of dag mutant leaves also lack their characteristic columnar shape. The DAG locus was cloned by transposon tagging: DAG encodes a novel protein with a predicted Mr of 26k, which is targeted to the plastids. Cleavage of its predicted transit peptide gives a mature protein of Mr 20k. Screening of databases and analysis of Southern blots gave evidence that DAG belongs to a protein family with homology to several proteins of unknown function from plants. Expression of DAG is required for expression of nuclear genes affecting the chloroplasts, such as CAB and RBCS, and also for expression of the plastidial gene RPOB encoding the plastidial RNA polymerase beta subunit, indicating that it functions very early in chloroplast development.

Amino Acid Sequence↗
PubMed1996

Differential effect of IFN-alpha and IFN-gamma on phosphorylation of p65 and p50 (rel) in the K562 cell line: implications for altered interaction with RXR beta.

Phosphorylation of nuclear transcription factors plays an important role in their ability to regulate genes in a differential manner. Recent studies indicate that the rel homology domain mediates interaction of rel proteins with other transcription factors. The rel domain is multiply phosphorylated. Thus, altered phosphorylation in this domain would affect synergy of rel proteins with members of other transcription factor families. This could affect differential expression of genes that are regulated by a combination of the two transcription factors. We have observed that in the K562 cell line IFN-alpha treatment leads to deficient phosphorylation of nuclear p65/p50 (rel). We propose that this prevents interaction between p65/p50 and RXR beta in IFN-alpha treated K562 cells. This could be a major reason for the lack of globin gene transcription by IFN-alpha.

Base Sequence↗
PubMed1996

Technetium-99m radiolabeled ouabagenin-cysteine conjugate: biological evaluation in animal models.

Two ouabagenin-cysteine conjugates were synthesized by condensing 3-beta monochloroacetyl and 3-beta, 11-alpha dichloroacetyl ouabagenin with cysteine. The resulting ligands were radiolabeled with technetium-99m (99mTc) to furnish a single homogenous 99mTc chelate in each case with good stability. The animal experiments with these 99mTc-labeled conjugates established the superiority of guinea pig over rat and rabbit as an animal model, as previously observed for other tritiated or radioidinated cardiac glycosides or aglycones. In biodistribution experiments in guinea pig, these 99mTc chelates showed a favorable heart to liver (and other nontarget organ) uptake ratio, comparable to that of recently reported 125I-digoxigenin iodohistamine-3-oxime. The low heart to blood ratio in animal experiments with ouabagenin derivatives could be attributed to the absence of 3-beta sugar residues in these molecules, which is in agreement with the previous observation reported in connection with radioiodinated digoxin and digoxigenin derivatives.

Animals↗
PubMed1996

Anomalies in hepatobiliary excretion of technetium-99m-MAG3 preparations.

Technetium-99m-MAG3 is accepted as a renal tubular function agent. However, sporadic liver and gall bladder visualisation during its clinical use is clearly a disadvantage. HPLC-purified 99mTc-MAG3 samples exhibited appreciable hepatobiliary uptake (7%), and an elevated level of such uptake was observed in unpurified kit preparations, which was stated to be associated with the excretory property of the radiolabeled kit impurities. To verify this we attempted to quantitate the hepatobiliary uptake of the kit preparations with that of its radiolabeled components. The contribution of each component toward hepatobiliary uptake of the sample was calculated from their abundance in the chelate mixture and the individual biodistribution of the isolated components. However, the anticipated hepatobiliary uptake of different preparations of 99mTc-MAG3 calculated in this way was always lower than that of the experimental value determined directly. Further work is needed to explain the anomaly.

Animals↗
PubMed1996

Antiplatelet and antiproliferative effects of SCH 51866, a novel type 1 and type 5 phosphodiesterase inhibitor.

SCH 51866 is a potent and selective PDE1 and PDE5 inhibitor. The antiplatelet, antiproliferative, and hemodynamic effects of SCH 51866 were compared with those of E4021, a highly selective PDE5 inhibitor. SCH 51866 inhibited PDE1 and PDE5 isozymes with a 50% inhibitory concentration (IC50) of 70 and 60 nM, respectively. SCH 51866 and E4021 inhibited washed human platelet aggregation induced by collagen with an IC50 of 10 and 4 microM, respectively, and attenuated (p < 0.05) the adhesion of 111indium-labeled platelets to the nylon filament-injured rat aorta. The doses of SCH 51866 and E4021 that inhibited platelet adhesion caused significant increases in platelet cyclic guanosine monophosphate (cGMP; p < 0.05). SCH 51866 (1-10 mg/kg, p.o. twice daily) but not E4021 (3-30 mg/kg, p.o twice daily) inhibited neointima formation in the carotid arteries of spontaneously hypertensive rats (SHRs) subjected to balloon angioplasty. Moreover, SCH 51866 (0.3-10 mg/kg, p.o.) elicited dose-dependent reduction in blood pressure in SHRs, whereas E4021 (3-30 mg/kg, p.o.) did not affect blood pressure in SHRs. In conclusion, the data suggest that inhibition of PDE1 and PDE5 isozymes by SCH 51866 exerts antiplatelet and vascular protective effects. In comparison, inhibition of PDE5 alone by E4021 exhibited antiplatelet effects without affecting neointima formation.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1996

Selenomethionine in the inhibition of a transplantable murine lymphoma: reflection on hepatic drug metabolizing enzymes.

This study attempts to determine whether selenomethionine treatment can improve the survival time of mice inoculated with Dalton's lymphoma (DL) and thereby to identify phase/phases of the neoplastic processes at which selenium exerts its maximal action as an anticancer agent. Accordingly, a maximum of 30.76 and 143% increase in survival was brought about by treatment of selenomethionine prior to lymphoma transplantation, in comparison to mice receiving selenomethione supplementation concurrently with inoculation of DL, and those tumor-bearing mice receiving no supplementation, respectively. Beneficiality of selenomethionine has also been studied by monitoring the continuous changes brought about by this compound on hepatic total cytochrome P-450 and b5 content, NADPH cytochrome c reductase, UDP glucuronyl transferase and glutathione S-transferase (GST) activities. These are important biotransformation enzymes and are altered significantly in neoplasia. The drastic increase in all the markers studied, excepting GST, was effectively counteracted by selenomethionine treatment (more before than concurrently), which sufficiently delayed and controlled the increase in those xenobiotic indices. The 112 and 78.78% induction in GST activity brought about by prior and concurrent treatment of selenomethionine, respectively, confirms the fact that inducers of GSTs are often antitumorigenic.

Animals↗
PubMed1996

Evidence for the presence of a proteinase-activated receptor distinct from the thrombin receptor in vascular endothelial cells.

The thrombin receptor was the first cloned G protein-coupled receptor reported to be activated by proteolytic cleavage of its extracellular amino terminus. A second proteinase-activated receptor (PAR-2) was cloned recently and expressed in Xenopus laevis oocytes. PAR-2 was activated by trypsin and by a peptide (SLIGRL) derived from the new amino terminus. Since PAR-2 mRNA was detected in highly vascularized organs, we compared the physiological functions of the thrombin receptor and PAR-2 in vascular endothelium. Thrombin and trypsin both elicited endothelium-dependent relaxations in prostaglandin F2alpha (PGF2alpha)-contracted strips of porcine coronary artery. Whereas high doses of both thrombin or trypsin (10 U/mL) caused homologous desensitization, trypsin caused further relaxation of thrombin-desensitized tissues. Thrombin and PAR-2-derived peptides (SFLLRN and SLIGRL) both induced endothelium-dependent relaxations in PGF2alpha-contracted porcine coronary arteries. SFLLRN or SLIGRL (30 micronmol/L) also showed homologous desensitization but not cross desensitization. In the presence of the NO synthase inhibitor NG-monomethyl-L-arginine (1 mmol/L), both SFLLRN- and SLIGRL-induced relaxations were partially inhibited. SFLLRN elicited weak contraction in coronary arteries without endothelium, whereas SLIGRL had no effect. Intravenous injection of SFLLRN (1 mg/kg, bolus) into anesthetized rats elicited a transient depressor response followed by pronounced pressor response. In contrast, intravenous administration of SLIGRL (1 mg/kg, bolus) produced only a marked depressor response. Consistent with the in vivo data, SFLLRN contracted the endothelium-rubbed rat aortic rings and aggregated human platelets in vitro, whereas SLIGRL had no effect. The finding that both trypsin and SLIGRL induced endothelium-dependent relaxations indicates the presence of PAR-2 on endothelial cells. In addition, both trypsin and SLIGRL elicited relaxations in thrombin- or SFLLRN-desensitized tissue, suggesting that PAR-2 is distinct from thrombin receptor in vascular endothelium. The lack of PAR-2-mediated platelet aggregation or smooth muscle contraction suggested it might not share the pathogenic properties associated with the thrombin receptor in the vasculature.

Animals↗
PubMed1996

Role of vitamin D3 on the activity patterns of hepatic drug metabolizing enzymes in transplantable murine lymphoma.

Vitamin D3 (D3) has been found to exert varied pharmacological actions including restriction of cell growth of a number of malignant cell lines in vitro and inhibition of the promotion of chemical carcinogenesis in mouse skin. In an attempt to confirm the efficacy of D3 as an antineoplastic agent, the present investigation aims at characterizing the importance of D3 in modulating hepatic drug metabolizing enzymes, namely, cytosolic glutathione S-transferase (GSHT), microsomal UDP glucuronyl transferase (UDPGT), and cytochrome P-450, which have been reported by us in recent literature as significant neoplastic markers in mice bearing Dalton's lymphoma (DL). Results show that D3 causes a 150% elevation of GSHT activity and the maintenance of normal, near-control UDPGT activity and cytochrome P-450 content, up to almost 30 days following tumor transplantation, along with bringing about a twofold increase in survival of the host mice. In conclusion, we confirm the definite and significant antitumorigenic role of D3 and its involvement with the discussed hepatic tumor markers in monitoring the processes that lead to cell survival.

Animals↗
PubMed1996

Comparative effectiveness of vitamin D3 and dietary vitamin E on peroxidation of lipids and enzymes of the hepatic antioxidant system in Sprague--Dawley rats.

The vitamin D-endocrine system has mostly been studied for its role in calcium and phosphorus metabolism and its possible role as an antioxidant has been neglected. This study attempts to elucidate the antioxidative properties of the prohormone with respect to vitamin E, a membrane antioxidant. Results herein show that D3 treatment brought about similar reduction in the extent of lipid peroxidation and induction in superoxide dismutase (SOD) activity, as with vitamin E supplementation. While selenium dependent glutathione peroxidase (Sedep. GPx) activity reflected no change with vitamin D3 treatment, total GPx activity was more significantly influenced by vitamin D3 than by vitamin E. The glutathione (GSH) content in the experimental rats also reflected similar changes. Vitamin E supplementation caused 8.57% increase in glutathione reductase (GR) activity, while vitamin D3 decreased the concerned enzymes activity by 11.11%. Vitamin D3 treatment also caused 25% increase in glucose 6-phosphate dehydrogenase (G6PD) activity. These data thus suggest that vitamin D3 may function as an antioxidant in the liver in vivo and illustrate an effectiveness higher than that observed with vitamin E supplementation.

Animals↗
PubMed1996

Biochemical basis of selenomethionine-mediated inhibition during 2-acetylaminofluorene-induced hepatocarcinogenesis in the rat.

Supplementation of selenium in the form of selenomethionine (8 ppm) in drinking water daily has been found to be highly effective in reducing cancer incidence in male Sprague-Dawley rats fed 2-acetylaminofluorine (2-AAF) (0.05%) in the basal diet daily for 16 weeks. Selenomethionine treatment before initiation, during initiation or during the selection/promotion phases of hepatocarcinogenesis has been found to be effective in elevating hepatic microsomal cytochrome b5, cytochrome P-450 contents, triphosphopyridine nucleotide-cytochrome c-reductase and cytosolic aryl hydrocarbon hydroxylase activities to a statistically significant level measured either in the hyperplastic nodules or in the non-nodular surrounding liver parenchyma compared with 2-AAF control rats. Moreover, selenomethionine treatment throughout the study also decreased the cytosolic 1-chloro-2,4-dinitrobenzene conjugated glutathione-S-transferase and microsomal UDP-glucuronyl transferase activities to a significant level when compared with 2-AAF control rats. Furthermore, direct correlations between hyperplastic nodules and non-nodular liver areas were observed with the hepatic selenium content and also with the rates and patterns of hepatic drug metabolism. Selenomethionine was also found to protect and improve the histopathological indices without any toxic side effects as revealed from the haematoxylin and eosin staining. Our results establish the fact that selenium is particularly protective in limiting the action of 2-AAF during the initiation phase of hepatocarcinogenesis.

2-Acetylaminofluorene↗
PubMed1996

Chemopreventive efficacy of selenomethionine and its role in the antioxidant defense system in 2-acetylaminofluorene-induced hepatocarcinogenesis in rats.

Drinking water supplemented with selenium (8 ppm, daily) has been found to be highly effective in reducing tumor incidence and preneoplastic foci in 2-acetylaminofluorene (2-AAF) induced hepatocarcinogenesis in Sprague-Dawley male rats. Glutathione and several enzymes in liver tissue associated with antioxidant defense mechanisms, viz., catalase, glutathione-S-transferase, glutathione peroxidase, glutathione reductase and superoxide dismutase were investigated from hyperplastic nodules and non-nodular surrounding parenchyma. Treatment with selenomethionine either on initiation, or on selection/promotion, or during the entire experiment showed that selenom-ethionine was most effective when it was used as a supplement during the entire experiment, in terms of the antioxidant defense system and in reducing tumor incidence. Our results also confirm that selenium is particularly effective in limiting the action of 2-AAF during the initiation phase of hepatocarcinogenesis.

2-Acetylaminofluorene↗
PubMed1995

Hepatoprotective activity of carrot (Daucus carota L.) against carbon tetrachloride intoxication in mouse liver.

The effect of carrot extract on carbon tetrachloride (CCl4)-induced acute liver damage was evaluated. The increased serum enzyme levels (viz., glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase, alkaline phosphatase, sorbitol and glutamate dehydrogenase) by CCl4-induction were significantly lowered due to pretreatment with the extract. The extract also decreased the elevated serum bilirubin and urea content due to CCl4 administration. Increased activities of hepatic 5'-nucleotidase, acid phosphatase, acid ribonuclease and decreased levels of succinic dehydrogenase, glucose-6-phosphatase and cytochrome P-450 produced by CCl4 were reversed by the extract in a dose-responsive way. Results of this study revealed that carrot could afford a significant protective action in the alleviation of CCl4-induced hepatocellular injury.

Alanine Transaminase↗