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Biomedical subjects

R K Upreti

Publications and source records attributed to R K Upreti.

At least 37 records · Page 2Linked to original sources
PubMed1992

Biochemical analysis of jejunal brush border membrane of golden hamster: pathogenic modulations due to ancylostomiasis.

The common hookworm (Ancylostoma ceylanicum) infection of humans was studied in golden hamsters model system. Significant biochemical modulations were observed in hamster jejunal brush border membrane (BBM), the primary site of infection. Analysis of BBM at the peak of infection (3-weeks) revealed a marked decrease in the activities of sucrase, lactase and maltase, while activities of alkaline phosphatase, (Ca2+ + Mg2+)-ATPase and gamma-glutamyl transpeptidase were increased. Kinetic studies conducted with maltase, a superficially localised enzyme of jejunal BBM, revealed loss of enzyme active site during the infection. Among other constituents, the levels of cholesterol and triglycerides were significantly decreased with slight increase in phospholipid content in the infected animals. The hookworm infection also caused a decline in total hexose content indicating an altered membrane glycocalyx. Conversely, there was significant enhancement of hydroxyproline and sialic acid contents. SDS-PAGE analysis showed an enhancement in both low and high molecular weight proteins in jejunal BBM preparations of the infected group. Gel electrophoresis of glycoproteins further revealed the appearance of two additional peaks in the low molecular weight region and concomitant disappearance of a peak in the high molecular weight region. These results strongly support the view that the hookworm infection causes severe damage not to the site of attachment alone but also to the entire cell lining of the jejunum and therefore could influence overall digestion and absorption.

Ancylostomiasis↗
PubMed1991

Membrane damaging potential of photosensitized riboflavin.

Riboflavin upon exposure to UV and visible radiations has been shown to produce active oxygen species. The present work deals with erythrocyte membrane as model system to study the damaging potential of photosensitized riboflavin. Membrane preparations (2.5 mg protein/ml) following exposure to sunlight in presence of riboflavin for different time intervals revealed significant inhibition of ATPases, p-nitrophenyl phosphatase and acetylcholinesterase. Considerable increase in lipid peroxidation was caused by the photosensitized riboflavin. Quenching studies using specific scavengers indicated remarkable inhibition. The production and identification of reactive oxygen species by photosensitized riboflavin and their possible involvement in membrane damaging effect has been discussed.

Erythrocyte Membrane↗
PubMed1990

An anorectic proteoglycan of membrane origin.

The endogenous substance(s) involved in the regulation of food intake has been isolated from serum, urine and feces. In the present study, a similar type of anorexigenic proteoglycan was isolated from human rat erythrocyte membranes and rat liver membranes. Membranes were suspended in 2.0% deoxycholate and allowed to stand at 25 degrees C for 30 min. The suspension was treated with 5% TCA, supernatant was collected, dialyzed and concentrated. TCA-soluble proteins were fractionated on Sephadex G-150. The active second peak fractions were further purified on DEAE-Sephadex A-25. Biologically active substance reduced the appetite in rats significantly when given intraperitoneally. The proteoglycan (50 kDa) consisted of 70-85% carbohydrate. Similar properties of plasma and membrane anorectic substance further indicated its membrane origin. We believe that this anorectic proteoglycan is anchored to cell membranes and released into the blood circulation to regulate the food intake.

Animals↗
PubMed1989

Dermal exposure to kerosene.

Young healthy albino male mice were subjected to repeated exposure to kerosene by wrapping each of their hind feet with a muslin cloth (1 x 10 cm) wetted with kerosene (0.1 ml). Exposure varied from 15 to 60 min/day for 7 consecutive days. Repeated exposure to kerosene produced histologic changes in the foot pad skin and popliteal lymph nodes of mice and systemic toxic manifestations such as variation in hematologic profile, significant decreases in relative weight of thymus, spleen and abdominal lymph nodes and altered histology. Three weeks of non-exposure rest indicated the reversible nature of kerosene-induced toxicity. Furthermore, observations made in 24 human subjects chronically exposed to kerosene in an automobile workshop revealed high incidence of oil acne and dermatitis of varying degrees. The study demonstrates a need for caution where ever prolonged dermal exposure to kerosene in occupational situations obtains.

Adult↗
PubMed1987

Interaction of di- and tributyltin chloride with human erythrocyte membrane.

Analysis of the binding of tributyltin chloride (TBT) to human erythrocyte membrane indicated a single class of binding site with an affinity of approximately 6.78 X 10(3) M-1, whereas dibutyltin dichloride (DBT) showed the presence of more than one class of binding sites with a high affinity value of 2.53 X 10(4) M-1 and a low affinity value of 2.06 X 10(3) M-1. Membrane protein binding studies revealed that both di- and tributyltin compounds bind significantly with band 3 protein of the erythrocyte membrane. These results indicate the significant interactions of erythrocyte membrane components with alkyltin compounds.

Erythrocyte Membrane↗
PubMed1987

2,5-Hexanedione-induced immunomodulatory effect in mice.

The immunotoxic potential of 2,5-hexanedione (2,5-Hxdn), the end metabolite of n-hexane/methyl n-butyl ketone, was evaluated in a mouse model involving multiple pathomorphological, hematological, and immunological assays. Young adult male Swiss albino mice were given either single or seven consecutive oral doses of 0.2 X LD50 of 2.5-Hxdn. None of the treated mice exhibited any sign of hind limb weakness up to 1 week. On the eighth day, half the animals were sacrificed for initial pathomorphological studies of various organs and the other half were subjected to several immune function tests. The results revealed treatment-related reduction in cellularity of spleen, thymus, and mesentric lymph nodes and pathotoxicological changes. Further, immune function tests such as delayed-type hypersensitivity reaction, plaque-forming cell assay, phagocytosis by adherent peritoneal exudate cells, and resistance to endotoxin shock were considerably impaired. These results suggest that 2,5-Hxdn treatment causes profound impairment of immunity in mice even before the onset of peripheral neuropathy.

Animals↗
PubMed1987

Isolation and characterization of basement membrane from frog skeletal muscle.

Isolation of basement membrane from frog skeletal muscle has been described. The membrane preparation contained 35 micrograms hexoses, 1.72 micrograms sialic acid, 6.8 micrograms phospholipids, 0.21 micrograms cholesterol/mg protein. Na + K-ATPase and 5'-nucleotidase could not be detected in the membrane preparation. Glycine accounted for about 20% of the total amino acids. On SDS-PAGE, the membrane resolved into 20-22 polypeptide bands.

Amino Acids↗
PubMed1986

Effect of 2,5-hexanedione on lymphoid organs of rats: a preliminary report.

Preliminary studies related to immunotoxicologic effects of 2,5-hexanedione, the final major metabolite of n-hexane/MnBk, were carried out in rats following single or repeated exposures. Female albino rats were given either single or seven consecutive oral doses of 0.1, 0.2, or 0.5 X LD50 of 2,5-hexanedione, and a time-related kinetic study was performed using hematology, histology, cellularity, and organ weight/body weight as major parameters. Following single exposure of 2,5-hexanedione to rats, a dose-dependent thymic atrophy was evident at the end of 7 days. The atrophy was reversible when the animals were given 7 days nonexposure rest. In contrast, there was no thymic atrophy when the animals were exposed for 7 consecutive days. Significant decline in the cellular populations of various lymphoid organs was also observed in rats exposed either to single or repeated doses of 2,5-hexanedione. Results obtained in the present study indicate that 2,5-hexanedione, a known potent neurotoxic substance, adversely affects the lymphoid organs of the immune system in rats.

Animals↗
PubMed1986

Influence of intraperitoneally administered formaldehyde on bile production and tissue glutathione levels in rats.

The influence of formaldehyde on bile secretion and tissue glutathione concentrations was investigated in male Sprague Dawley rats following a sublethal intraperitoneal administration (72 mg/kg). Within 2-3 h of administration formaldehyde caused a 2-fold increase in secretion of bile and significant decrease in the levels of glutathione in liver (39% of control) followed by kidney (33%), lung (31%) and brain (22%). The results indicate a possible protective role of glutathione in the toxicity of formaldehyde.

Animals↗
PubMed1983

Comparative toxicokinetics of 2,3-14C-and 1-14C-acrylonitrile in the rat.

The tissue distribution, elimination and covalent binding of 2,3-14C-and 1-14C-acrylonitrile (VCN) were studies in male Sprague-Dawley rats given an oral dose of 46.5 mg kg-1. Exhalation of unchanged VCN, 14CO2 and H14CN was monitored at selected intervals. Only 5% of the total dose administered was recovered was unchanged VCN. Rate given 2,3-14C-VCN exhaled only 2% of 14C activity was 14CO2 and none was recovered as H14CN, whereas rats given 1-14C-VCN exhaled about 12% of 14C activity as 14CO2 and 0.5% as H14CN. In the initial 24 h, 40% of radioactivity from 1-14C-VCN appeared in urine, while 60% was recovered in the urine of rats given 2,3-14C-VCN. The red blood cells retained significant amounts of radioactivity from both the compounds for more than 10 days after administration, whereas the 14C activity in plasma declined sharply. The highest level of radioactivity from both compounds was recovered in the gastrointestinal tract. In liver, kidney, brain, spleen, adrenal, lung and heart tissues the unbound percent radioactivity decreased, while irreversible percent covalent binding to macromolecules in relation to total increased concomitantly. Subcellular fractionation of the tissues showed that most of the covalently bound radioactivity was distributed in non-cytosolic fractions. As compared to 1-14C-VCN administered animals, the percentage of covalent binding of 2,3-14C-VCN was significantly higher even 72 h after dosing. The relationship between covalent binding and acrylonitrile toxicity is discussed.

Acrylonitrile↗
PubMed1982

Distribution and covalent interactions of [1-14C]acrylonitrile in the rat.

The tissue distribution, elimination and covalent binding of [1-14C]-acrylonitrile (VCN) have been investigated in the rat. Rats, given an oral dose of 46.5 mg/kg (0.5 LD50) VCN, excreted 40% of the 14C in urine, 2% in feces, 9% in expired air as 14CO2, 0.5% as H14CN and 4.8% as unchanged VCN in 24 h. Bile flow increased 3 times after the administration of VCN and over a period of 6 h, 27% of the 14C was recovered in bile. The red blood cells retained significant amounts of radioactivity for more than 10 days after treatment, whereas the 14C activity declined sharply in plasma. Initially, the highest levels of radioactivity were found in the stomach and stomach content followed by the intestine. In liver, kidney, brain, spleen, adrenal, lung and heart tissues the radioactivity of the acid soluble fractions declined while covalent binding to macromolecules remained unchanged. In subcellular fractions of liver, kidney, spleen, brain, lung, and heart, 20-40% of the total radioactivity was bound to nuclear, mitochondrial and microsomal fractions whereas in cytosol only 6-14% was bound over a period of 6 h.

Acrylonitrile↗