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Biomedical subjects

R Bhattacharya

Publications and source records attributed to R Bhattacharya.

At least 55 records · Page 3Linked to original sources
PubMed1995

Therapeutic efficacy of sodium nitrite and 4-dimethylaminophenol or hydroxylamine co-administration against cyanide poisoning in rats.

1. The therapeutic efficacy of combined treatment of sodium nitrite (NaNO2) and 4-dimethylaminophenol (DMAP) or hydroxylamine (H2NOH) was investigated in potassium cyanide (KCN) intoxication in male rats. 2. Therapy with NaNO2 (0.27 mmol kg-1) + DMAP (0.09 mmol kg-1) or NaNO2 + H2NOH (0.09 mmol kg-1, produced a protection index (ratio of LD50 of KCN in rats receiving therapy to an LD50 of KCN in rats given only 0.9% saline) of 2.5 and 2.0 respectively. 3. Both the regimens exhibited a beneficial effect in terms of improving the survival time and postural defects in rats exposed to 2 LD50 KCN. 4. NaNO2 + DMAP showed a significant protective effect in the disposition of the plasma cyanide level at different time intervals. 5. The NaNO2 + DMAP regimen was superior to NaNO2 + N2NOH in terms of reactivating the inhibited brain cytochrome oxidase enzyme. 6. The addition of sodium thiosulphate (Na2S2O3) in both the regimens increased the degree of protection. 7. The results suggest that combined therapy with NaNO2 + DMAP could significantly reduce the toxic effects of cyanide, compared with NaNO2+H2NOH treatment.

Aminophenols↗
PubMed1995

Toxicity evaluation of in vitro cultures of freshwater cyanobacterium Microcystis aeruginosa: I. Hepatotoxic and histopathological effects in rats.

Laboratory cultures of freshwater cyanobacterium (blue-green alga) Microcystic aeruginosa PCC 7806 was evaluated for its hepatotoxic effects in rats. The lyophilized cell extract injected intraperitoneally at 1 and 2 LD50 (15.8 and 31.6 mg/kg, respectively) produced significant increase in liver-specific enzymes viz. plasma alkaline phosphatase, gamma-glutamyl transferase, lactate dehydrogenase with a concomitant decrease in hepatic glutamic pyruvic transaminase. A corresponding increase in liver body weight index and histopathological changes in liver (degeneration of hepatocytes, congestion and hemorrhage etc.) are indicative of a dose and time dependent hepatotoxic nature of the algal extract.

Alanine Transaminase↗
PubMed1994

Human erythrocyte membrane protein 4.2 is palmitoylated.

Protein 4.2 is a major protein of the human erythrocyte membrane. It has previously been shown to be N-myristoylated. After labeling of intact human erythrocytes with [3H]palmitic acid, radioactivity was found to be associated with protein 4.2 by immunoprecipitation of peripheral membrane proteins extracted at pH 11 from ghosts with anti-(4.2) sera, followed by SDS/PAGE and fluorography. The fatty acid linked to protein 4.2 was identified as palmitic acid after hydrolysis of protein and thin-layer chromatography of the fatty acid extracted in the organic phase. Protein 4.2 could be depalmitoylated with hydroxylamine, suggesting a thioester linkage. Depalmitoylated protein 4.2 showed significantly decreased binding to protein-4.2-depleted membranes, compared to native protein 4.2.

Blood Proteins↗
PubMed1994

Dose-dependent effects of zinc supplementation during chelation of lead in rats.

Dose-dependent effects of zinc supplementation in order to enhance the efficacy of calcium disodium EDTA in lead intoxicated rats was investigated in rats. The results suggest simultaneous supplementation of zinc at a lower concentration i.e. 10 mg/kg (orally, once during chelation treatment), 25 mg/kg zinc (Flora & Tandon 1990) potentiates the mobilization of lead from blood and soft tissues. However, at a higher dose level (50 mg/kg once orally) it has deleterious and much reduced ability to deplete tissue lead contents and restore altered lead sensitive biochemical variables.

Animals↗
PubMed1994

Cyanide induced changes in dynamic pulmonary mechanics in rats.

Effect of subcutaneously (s.c.) administered potassium cyanide (0.5 and 1.0 LD50) and inhalation of hydrogen cyanide (55 ppm or 60.6 mg/m3) for 30 minutes was studied on various physiological parameters related to dynamic pulmonary mechanics in anaesthetized rats. Total pulmonary phospholipid with its fractions were also estimated. Both s.c. (1.0 LD50) and inhalation exposures increased air flow, transthoracic pressure and tidal volume accompanied by significant decrease in pulmonary phospholipids. Inhalation of hydrogen cyanide also exhibited direct effect on the pulmonary cells as evidenced by decreased compliance. The study suggests that inhalation of cyanide is more injurious compared to parenteral route.

Animals↗
PubMed1994

Effect of rehydrating fluid 'Electral' on Vibrio cholerae cells.

V. cholerae OGAWA 154 cells underwent rapid loss of colony forming capacity during the first few minutes' incubation in the Electral medium at 37 degrees C, the turbidity of the suspension however increasing with time of incubation and leading to a plateau from 5 min onward. The vibrio suspension in the Electral medium released small amounts of 280 nm and much higher amounts of 260 nm absorbing materials. On withdrawal of the Electral medium, the cells underwent significant liquid holding recovery in the phosphate buffered saline, pH 7. Majority of the cells underwent no significant ultrastructural change but grew into long filamentous forms. The mode of action of the Electral medium on the vibrios is discussed.

Rehydration Solutions↗
PubMed1993

Protection against cyanide poisoning by the co-administration of sodium nitrite and hydroxylamine in rats.

1. The protectiveness of combined treatment with sodium nitrite (SN) and hydroxylamine (HA) in cyanide intoxication was investigated in male rats. 2. Pretreatment with equimolar dose of SN or HA produced a significant protection against cyanide poisoning as shown by the protection index (LD50 of cyanide in protected rats/LD50 of cyanide in saline-treated rats). 3. The co-administration of SN and HA as a split dose produced an optimal and sustained methaemoglobinaemia. 4. Pretreatment with combined SN and HA administration at different time intervals offered sustained protection against cyanide and resultant cytochrome oxidase inhibition. 5. Adjunction of sodium thiosulphate (STS) in the SN+HA regimen further augmented the protection against cyanide poisoning. 6. The results suggest that pretreatment with SN+HA co-administration could significantly reduce the toxic manifestation of cyanide.

Animals↗
PubMed1993

Effects of nitrofurantoin on viability, DNA synthesis and morphology of Vibrio cholerae cells.

Nitrofurantoin caused a dose dependent inhibition of growth and decrease in viability of V. cholerae cells, the 10% (D10) and 37% (D37) survival doses being 50 and 19 micrograms/ml respectively. The drug at a concentration of 60 micrograms/ml caused 86% inhibition of DNA synthesis. Both light and electron microscopic observations revealed that treatment with nitrofurantoin (60 micrograms/ml for 1 hr at 37 degrees C) led to a significant filamentation of the V. cholerae cells, ultrastructure of the cell cytoplasm, plasma membrane and cell wall however remaining unaltered from those of untreated cells. The results are discussed in relation to DNA lesions produced by and the carcinogenic potential of the drug.

Cell Division↗
PubMed1992

The 3,3'-bis-pyridinium mono-oximes as antidotes against organophosphorous intoxication.

In an attempt to develop effective antidotes against organophosphorous intoxication, three new structurally related bispyridinium mono-oximes with a 2-oxopropane bridge were synthesized. The compounds were evaluated for in-vivo therapeutic protection and cholinesterase reactivation in blood and various brain regions. In neuromuscular function studies against diisopropyl-fluorophosphate and isopropyl methylphosphonofluoridate poisoning, the oximes produced significant protection. The compounds produced marked peripheral reactivation and beneficial effects on neuromuscular transmission. The reactivation of cholinesterase in cerebral cortex by the oximes, in spite of their being quaternary salts is a notable feature.

Animals↗
PubMed1992

Biochemical changes induced by two new prophylactic regimens for cyanide antagonism.

Clinical efficacy of two pretreatment regimens, sodium nitrite (SN) + hydroxylamine (HA) and SN + 4-dimethylaminophenol (DMAP) were evaluated in rats by studying various biochemical variables at different time intervals. Animals given single subcutaneous (s.c.) co-administration of SN+HA or SN+DMAP showed significantly elevated levels of blood bilirubin indicating hemolytic anemia. Increased levels of blood creatine phosphokinase (CPK), lactate dehydrogenase (LDH) and glutamic oxaloacetic transaminase (GOT) were indicative of aseptic necrosis at the injection site. On account of low methemoglobin reductase activity in human erythrocytes, a reduced sub-clinical dose of HA or DMAP is envisaged in humans.

Aminophenols↗
PubMed1991

Acute toxicity of methyl isocyanate in mammals. IV. Biochemical and hematological changes in rabbits.

Subcutaneous administration of methyl isocyanate (MIC) in 0.5 LD50 and 1.0 LD50 to female rabbits resulted in significant increases of hemoglobin concentration, hematocrit and leukocyte count in blood, as well as plasma total proteins, urea and cholesterol. A significant decrease in plasma albumin level was only observed in the 1.0 LD50 group. Urine of MIC intoxicated animals showed presence of protein, bilirubin, elevated urea and urobilinogen, while urine volume was reduced. The hematological and biochemical changes induced by MIC are perhaps the result of fluid loss from the vascular compartment as evidenced by the histopathological observations. This study further substantiates the view that acute toxicity of MIC is mediated in vivo by its effects on vascular beds.

Animals↗
PubMed1991

Cyanide intoxication in mice through different routes and its prophylaxis by alpha-ketoglutarate.

Antagonising effects of alpha-ketoglutarate (alpha-KG) could be attributed to complexing of the reactive nucleophile (CN-) to form cyanohydrin in cyanide intoxication. However, an enormous protection obtained could not be delineated on account of possible in situ binding of alpha-KG given intraperitoneally (i.p.) in mice to cyanide administered through the same route. The present study was designed to see the efficacy of alpha-KG alone or in combination with sodium nitrite (SN) and/or sodium thiosulfate (STS) in male mice exposed to cyanide administered through subcutaneous (s.c.) or inhalation route. A technique for generation of hydrogen cyanide (HCN) is also discussed. On the basis of protection index (PI), defined here as the LD50 of cyanide in protected mice/LD50 of cyanide in unprotected mice and survival time, STS + alpha-KG regimen was equipotent to the conventional SN + STS regimen. This is further substantiated by effect of alpha-KG in reducing plasma cyanide levels. The efficacy of alpha-KG remains undeterred irrespective of the route of cyanide intoxication, while the magnitude of protection varies.

Animals↗