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Biomedical subjects

C Dwivedi

Publications and source records attributed to C Dwivedi.

At least 37 records · Page 2Linked to original sources
PubMed1990

Antineoplastic properties of Maharishi-4 against DMBA-induced mammary tumors in rats.

Maharishi-4 (M-4), an ayurvedic food supplement, was tested for anticarcinogenic and anticancer properties against 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary tumors in rats. The 6% M-4-supplemented diet protected DMBA-induced carcinogenesis by reducing both tumor incidence and multiplicity during initiation and promotion phases. The control animals who developed tumors when supplemented with M-4 diet for four weeks showed tumor regression in 60% of cases. There was no significant difference in the food intake or weight gain in rats who were on M-4-supplemented diet compared to control group. Possible mechanisms of action of M-4 are discussed.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1990

Effect of calcium glucarate on beta-glucuronidase activity and glucarate content of certain vegetables and fruits.

Glucarate is normally present in tissues and body fluids and is in equilibrium with D-glucaro-1,4-lactone, a natural inhibitor of beta-glucuronidase activity. Dietary calcium glucarate, a sustained-release from of glucarate, elevates the blood level of D-glucaro-1,4-lactone which suppresses blood and tissue beta-glucuronidase activity. A single dose of CaG (4.5 mmole/kg body weight) inhibited beta-glucuronidase activity in serum and liver, lung, and intestinal microsomes by 57, 44, 37, and 39%, respectively. A chronic administration of calcium glucarate (4% in diet) also decreased beta-glucuronidase activity in intestinal and liver microsomes. Maximal inhibition of beta-glucuronidase activity in serum was observed from 12 noon to 2:00 PM. In contrast, maximum inhibition of beta-glucuronidase activity in intestinal and liver microsomes occurred during mornings, although a secondary depression in intestinal microsomes also occurred around 4 PM. A 4% calcium glucarate supplemented diet also inhibited beta-glucuronidase activity by 70% and 54%, of the bacterial flora obtained from proximal (small intestine) and distal (colon) segments of intestine, respectively. Due to the potential effect of dietary glucarate on net glucuronidation and on other metabolic pathways, glucaric acid levels in various foods were determined. The glucaric acid content varied from a low of 1.12-1.73 mg/100 g for broccoli and potatoes to a high of 4.53 mg/100 g for oranges.

Animals↗
PubMed1989

Effect of cholinergic agents on human spermatozoa motility.

The effect of various cholinergic agents on human spermatozoa motility was studied. Both direct-acting (e.g., acetylcholine, pilocarpine) and indirect-acting (e.g., physostigmine) cholinergic agonists stimulated human spermatozoa motility. All the cholinergic antagonists (e.g., atropine, hyoscine, hexamethonium, d-tubocurarine, and succinylcholine) inhibited the spermatozoa motility. At 1 X 10(-4) M, muscarinic antagonists, atropine and hyoscine, did not influence motility, whereas nicotinic antagonists, hexamethonium, d-tubocurarine and succinylcholine, depressed motility. These observations suggest that a nicotinic-type receptor is present in spermatozoa. However, these studies did not exclude the possibility of the presence of a muscarinic receptor in spermatozoa.

Adult↗
PubMed1989

Effects of the experimental chemopreventative agent, glucarate, on intestinal carcinogenesis in rats.

Dietary calcium glucarate was previously shown to protect effectively against chemically-induced mammary, lung, liver and skin carcinogenesis in rodents, whereas the negative dietary calcium control, calcium gluconate, had no effect. In the present study the chemopreventative activity of dietary calcium glucarate was evaluated in the azoxymethane intestinal carcinogenesis model using the Fischer strain rat. The protocol limited the duration of azoxymethane treatment to 3 weeks to permit the evaluation of the separate effects of glucarate on the initiation and promotion phases. Control rats, treated with azoxymethane and maintained on a low fat chow diet throughout the 32-week experiment had an intestinal adenocarcinoma incidence of 55%, with an equal incidence of 27.7% in the small and large intestines. There was no significant difference between this control group and a negative calcium control group fed 128 mmol/kg chow of calcium as calcium gluconate. In contrast to these two control groups, supplementation of the diet of azoxymethane-treated rats with 128 mmol/kg diet of calcium glucarate during both the initiation and promotion phases significantly inhibited the overall induction of adenocarcinomas in the intestine, the incidence in the entire intestine and in the small and large intestines being 11.8, 5.8 and 5.8%, respectively. When fed only during the initiation phase, the inhibition again was statistically significant, the corresponding values being 11.8%, 5.8 and 5.8%. When calcium glucarate was fed during the promotion phase, a statistically significant inhibition of adenocarcinoma induction was observed only in the colon where the incidence was 5.5%. Weight gain was similar in all groups. These and related data indicate that dietary glucarate exerts a significant inhibitory effect on azoxymethane-induced intestinal and in particular colon carcinogenesis in the rat, decreasing their incidence and size and reducing their metastic potential.

Animals↗
PubMed1989

Chemopreventative activity of dietary glucarate on azoxymethane-induced altered hepatic foci in rats.

Previous studies have shown that dietary calcium glucarate, an inhibitor of beta-glucuronidase, is a potent inhibitor of promotion of diethylnitrosamine-induced altered hepatic foci, 7,12-dimethylbenzanthracene-induced mammary tumorigenesis and benzo(a)pyrene-induced lung carcinogenesis. The present study was undertaken to test the chemopreventative activity of calcium glucarate on azoxymethane-induced hepatocarcinogenesis in female Fischer 344 rats. A series of experiments were carried out over 36 weeks to evaluate the effects of calcium glucarate on the initiation and promotion phases separately and also in combination with each other. A calcium gluconate group was included and used as a negative calcium control. Histopathologic evaluation of H&E stained liver sections of all animals in this study showed that a statistically significant inhibition of hepatocarcinogenesis only occurred when dietary calcium glucarate supplementation was provided throughout the combined initiation and promotion phases. This inhibitory effect approximately equaled the summation of that obtained when calcium glucarate was fed only during initiation phase and only during promotion phase.

Animals↗
PubMed1988

Fibrin activatable urokinase (FA-UK): a latent form of UK found in urine related to a complex with an inhibitor/fibrin-interacting cofactor.

In order to investigate the binding of pro-urokinase (pro-UK) in urine to fibrin/Celite, the property which led to its discovery, the effect of fibrin on the plasminogen activator activity of urine was studied. The plasminogen activator activity in urine was found to be consistently about 2-fold higher when measured by fibrin plate assay than by amidolytic substrate (S-2444), when normalized against the UK reference standard. When the amidolytic activity measurement was preceded by incubation of urine with soluble fibrin, a 2-fold increase in amidolytic activity was also found. Fibrin similarly increased plasmin generation in urine enriched with Glu- or Lys-plasminogen as determined by synthetic substrate S-2251. The observed promoting effect was common to several forms of soluble fibrin and was dose dependent, whereas fibrinogen had little effect. The promoting effect of fibrin was not expressed in the presence of pro-UK or two-chain UK (TC-UK) in buffer and therefore was attributed to another constituent of urine. Since the activity was inhibited by antibodies to UK but not to t-PA, it was called fibrin activatable UK (FA-UK). Gel filtration (Sephacryl-200) of urine revealed FA-UK activity in fractions eluting at a molecular weight of approximately 100K. A 100 K band of activity was also consistently seen when concentrated urine was subjected to zymography. Treatment of concentrated urine with hydroxylamine (1 M) eradicated both these activities and was associated with an increase in baseline amidolytic activity in the urine sample indicative of the release of UK from an inhibitor complex. Moreover, passage of urine over insolubilized monoclonal antibody against UK-inhibitor (PAI-3) complexes resulted in loss of FA-UK activity and of the 100 K band on the zymogram suggesting that the complex responsible for FA-UK was related to a PAI-3 complex. Since the FA-UK activity appeared to bind to fibrin/Celite, attempts were made to investigate complexation with pro-UK. Unfortunately, due to the instability of pro-UK in urine, no reliable data were obtained. It was concluded that PAI-3 may serve as a fibrin-interacting co-factor of UK, and therefore may play a role in fibrinolysis.

Antibodies, Monoclonal↗
PubMed1988

Putative metabolites derived from dietary combinations of calcium glucarate and N-(4-hydroxyphenyl)retinamide act synergistically to inhibit the induction of rat mammary tumors by 7,12-dimethylbenz[a]anthracene.

Calcium glucarate and N-(4-hydroxyphenyl)retinamide were evaluated individually and in combination in the diet as preventative chemical agents, by using the induction of rat mammary tumors by 7,12-dimethylbenz[a]anthracene as the test system. When tested separately over 18 weeks, optimal doses of calcium glucarate (128 mmol/kg of diet) or N-(4-hydroxyphenyl)retinamide (1.5 mmol/kg of diet) administered daily inhibited tumor incidence by 50% or 57% and tumor multiplicity by 50% or 65%, respectively. Suboptimal doses of calcium glucarate (32 mmol/kg) and of N-(4-hydroxyphenyl)retinamide (0.75 mmol/kg) inhibited tumor incidence by 15% and 5% but had no inhibitory effect on tumor multiplicity. In contrast, the combination of calcium glucarate (32 mmol/kg) and N-(4-hydroxyphenyl)retinamide (0.75 mmol/kg) inhibited tumor incidence and tumor multiplicity by 50%. Similar synergism was observed with the combination of calcium glucarate (64 mmol/kg) and N-(4-hydroxyphenyl)retinamide (0.75 mmol/kg), the inhibition being 55-60%. HPLC analysis of the bile of female rats injected intraperitoneally with a single dose of the retinamide [60 mg/kg (body weight)] showed that the excretion of the retinamide and its glucuronide were markedly suppressed by pretreatment with an oral dose of calcium glucarate [4.5 mmol/kg (body weight)].

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1988

Plasma sialyltransferase as a tumor marker.

Neoplastic transformations are accompanied by an alteration in the composition of cell membrane glycoproteins, major structural components of the cell surface. Plasma sialyltransferase enzyme is involved in the transfer of sialic acid residues from cytosine monophosphate (CMP) sialic acid to a suitable acceptor. In the present study plasma sialyltransferase was assayed using a radiometric method, which measured the transfer of radioactivity from (14C) CMP sialic acid to desialated fetuin. Plasma sialyltransferase was measured in 127 normal and 91 cancer patients. The mean plasma sialyltransferase in the normal volunteers was 837 units (CPM/25 microliters plasma/hr). The mean plasma sialytransferase in 26 breast cancer patients, 22 lung cancer patients, 20 colon cancer patients, 5 ovarian cancer patients, 4 cervix cancer patients, 5 pancreas cancer patients, 6 prostate cancer patients, and 3 gastrointestinal tract cancer patients was 1710, 1406, 1344, 1227, 1233, 1406, 1250, and 1426 units, respectively. No significant difference was observed with respect to age. In 32 treated breast cancer patients the mean value was 757 units. Serial determinations in 17 patients correlated well with tumor burden. However, in 2 patients the plasma enzyme level did not correspond to tumor mass. These results indicate that plasma sialyltransferase is significantly elevated in patients with a variety of cancers. Plasma sialyltransferase determination may be useful in the followup of patients with a variety of cancers.

Age Factors↗
PubMed1987

Net glucuronidation in different rat strains: importance of microsomal beta-glucuronidase.

The net glucuronidation of bilirubin (BR) has been determined in inbred and outbred rat strains and their subpopulations with similar glucuronosyltransferase (EC 2.4.1.17) activity but with different levels of beta-glucuronidase (beta G) (EC 3.2.1.31), or in which the level of beta G activity was reduced with D-glucaro-1,4-lactone. These studies demonstrated that outbred rat strains consist of two subpopulations that differ approximately 1.5- to two-fold in serum and liver beta G activity. Evidence is presented indicating that owing to its compartmentalization the lysosomal beta G, unlike the corresponding microsomal enzyme, is neither inhibited by glucarolactone nor accessible for hydrolysis of newly synthesized glucuronides. The ratio of glucuronidated to unconjugated BR 15 min after injection of albumin-bound BR into the tail vein appears to correlate negatively with the liver microsomal beta G activity. The results may be relevant to the relative risk to toxins, including carcinogens, and to their reduction by dietary intervention.

Animals↗
PubMed1987

Dithiocarbamate inhibition of cadmium-induced changes in spermatozoan acetyltransferases.

The administration of sodium N-methyl-N-dithiocarboxy-D-glucamine (NaG) subsequent to the administration of CdCl2.2.5H2O to male rats, inhibits the cadmium-induced decreases in spermatozoan acetyltransferase (AT) levels and provides marked protection against the cadmium-induced morphologic testicular changes in the cauda and corpus and partial protection against the changes in the caput.

Acetyltransferases↗
PubMed1987

Plasma sialic acid alterations in neoplastic diseases.

The several types of neoplastic transformations are accompanied by alterations in the composition of cell glycoproteins, which are major structural components of cell surfaces. One such observed alteration is in the level of sialic acid on the cell surface. In the present investigation, plasma sialic acid levels were measured in normal volunteers and neoplastic patients using thiobarbituric acid spectrophotometric methods. The mean plasma sialic acid level from 124 normal volunteers was 3.0 mumol/ml. The mean for 20 non-malignant patients was 3.2 mumol/ml. Such observed mean values of sialic acid were 3.7 mumol/ml in 64 breast cancer patients, 5.1 mumol/ml in 22 lung cancer patients, 4.1 mumol/ml in 20 colon patients, and 5.0 mumol/ml in 26 patients having ovarian, cervix, pancreas, prostate, thyroid, uterine, squamous cell, esophageal and endometrial cancers. Serial determinations of plasma sialic acid in 15 patients correlated well with the progression and regression of disease. These results indicate that plasma sialic acid levels are elevated over control levels in the different types of cancer patients studied. Assay of plasma sialic acid is not sensitive enough to be used for screening, but could be used as a prognostic determinant in a variety of neoplastic conditions.

Age Factors↗
PubMed1986

Effects of abnormal metabolites of maple syrup urine disease on neurotransmitter receptor binding.

The deficiency of keto acid decarboxylase in maple syrup urine disease results in the accumulation of branched chain amino acids and their corresponding keto acids in tissues and body fluids. The effects of abnormal metabolites were investigated on neurotransmitter receptor binding in rat brain. alpha-Keto acids caused selective in vitro decrease in alpha-adrenergic, beta-adrenergic receptor binding in synaptosomal preparations from rat brain. No significant changes were observed in binding of cholinergic, GABA, and dopamine receptors binding in appropriate rat brain preparations. These results indicate that selective inhibition of adrenergic receptor binding by branched chain keto acids may presumably account for neural abnormality in maple syrup urine disease.

Amino Acids, Branched-Chain↗
PubMed1986

Vaso-occlusive crisis episodes in sickle cell disease.

Seventeen adult males and females with Hb-SS, Hb-SC (1) and Hb-S Thal (1) hemoglobinopathies were continuously studied for 3 years. Various hematological and biochemical parameters were measured in the venous blood of the subjects for blood gases, CBC profile, blood chemistry (SMA-18), fibrinogen, alpha-HBD and myoglobin levels, percent sickling, blood viscosity, oxygen affinity of whole blood, osmofragility of red blood cells and calcium and zinc contents in plasma and in RBC. The results were compared between those subjects who encountered more frequent vaso-occlusive crisis episodes (frequent sicklers) and those with fewer crisis episodes (infrequent sicklers), along with parameters between crisis and non-crisis states of frequent sicklers. Our studies showed that percent sickling, P50 for O2, CBC profile, PO2, serum calcium, ALP, LDH, alpha-HBD level, zinc and calcium levels in plasma and in RBC varied between crisis and non-crisis states of frequent sicklers and also between frequent sicklers and infrequent sicklers. A logical explanation of such variations may help in understanding the etiology of vaso-occlusive crisis episodes in sickle cell disease.

Adult↗
PubMed1984

Correlation between plasma carcinoembryonic antigen (CEA) and sialyltransferase as tumor marker.

Plasma carcinoembryonic antigen (CEA) and sialyltransferase levels were assayed in 21 cancer patients to correlate them in response to therapy. Plasma sialyltransferase and CEA level correlated well in 10 colon, 4 breast and 1 lung cancer patients in response to therapy. There was a negative correlation in one colon cancer, 3 breast cancer and 2 lung cancer patients. Plasma sialyltransferase was a better marker for breast and lung cancer. CEA was a good marker for colon cancer.

Breast Neoplasms↗
PubMed1983

Diagnostic use of cerebrospinal fluid lactic acid levels in meningitis.

Analysis of cerebrospinal fluid lactic acid levels in 62 patients suspected of having meningitis was performed. Lactic acid was measured enzymatically using lactic acid dehydrogenase with the liberation of NADH. In a control (no meningitis) group, 46 children had a mean cerebrospinal fluid lactic acid level of 14.7 +/- 2.2 mg/dl; 3 with febrile seizure had a mean lactic acid level of 33.5 +/- 0.98 mg/dl. In 9 cases of bacterial meningitis, the mean lactic acid level was 54.8 +/- 16.8 mg/dl. In 3 patients of aseptic meningitis, the mean lactic acid level was 34.5 +/- 1.0 mg/dl. Serial lactate determination was done in three patients and they were well correlated with the clinical response and other cerebrospinal fluid findings. These data suggest that the determination of cerebrospinal fluid lactic acid may be of diagnostic value in differentiating between bacterial and aseptic meningitis.

Adolescent↗
PubMed1982

Choline acetyltransferase activity during postnatal development of the rat heart.

Choline acetyltransferase (ChAT), the enzyme which catalyze the synthesis of acetylcholine is present in rat heart tissue on the first day of life. ChAT activity increases with age and reaches to a peak of adult level at the age of 40 days. Chat activity was highest in the right atrium then in right ventricle followed by left ventricle and left atrium. These preliminary results suggest that balanced control of the heart by autonomic nervous system is not complete at birth and is at certain risk.

Aging↗