Biomedical subjects
Publications and source records attributed to S Chaudhury.
In a study of 100 institutionalised patients with psychosis and an equal number of age- and sex-matched healthy controls from the same regional background, the prevalence of Australia antigen (HBsAg) was 11 and 2, respectively. Institutionalised psychotic patients are a high-risk group for hepatitis B virus infection.
Effect of group IIB metals on the endogenous status of metallothionein (MT) and reduced glutathione (GSH) was studied in two vital detoxifying organs namely, liver and kidney of rat. The metals were administered at non lethal levels (1/10 LD50) which were found to cause no death. Zinc showed accumulation in both liver and kidney, cadmium preferentially in the liver while mercury in the kidney. Hepatic MT content was increased by 18-fold, 15-fold and 2-fold by cadmium, zinc and mercury respectively while renal MT was increased maximally by zinc. Among the metals, mercury caused highest depletion of hepatic GSH level (51%). The renal GSH showed differential response to the metal treatment, the level increasing slightly by cadmium and depleting significantly by zinc and mercury. A positive correlation was found between group IIB metal accumulation and the manifestation of toxic response.
One-hundred-seventy-nine lepromin-negative household contacts were vaccinated with heat-killed Mycobacterium leprae, BCG, or a combination of the two. Vaccination induced lepromin positivity in 131 of these contacts. Over an 8-year follow-up period, 12 lepromin-positive contacts developed leprosy, all tuberculoid; while 2 lepromin-negative vaccinated contacts developed leprosy, both lepromatous. Overall, 7.8% of the vaccinated contacts developed the disease. Seven-hundred-fourteen household contacts were not vaccinated, and served as controls. Among the 504 who were lepromin positive, leprosy developed in 35, all tuberculoid, over the 8-year follow up. Among the 210 lepromin-negative unvaccinated contacts, 61 developed leprosy: tuberculoid in 29, borderline in 4, lepromatous in 8, and indeterminate in 20. Overall, 13.5% of the 714 unvaccinated contacts and 29.0% of the 210 unvaccinated, lepromin-negative contacts developed leprosy. Vaccination could not induce lepromin positivity in all contacts. The three vaccines were equally effective in inducing lepromin positivity. Vaccination reduced the overall incidence of leprosy from 13.5% to 7.8% among household contacts but did not reduce the incidence of lepromatous leprosy (1.2% of all the vaccinated and 1.1% of all the unvaccinated contacts).
The role of reproductive factors, such as, parity, age at menarche, age at first child's birth have been investigated in a hospital based case-control study, for their independent as well as combined influences on the incidence of female breast cancer. The study indicates that except for parity, these factors have no influence on the age at onset of the disease. Parity is positively correlated with age at onset. The patient and the control groups were found to be similar in respect of age at first child's birth and age at menarche, but the patient group was significantly lower both in parity and age at onset of the disease. Both these factors are negatively associated with the incidence of breast cancer. Therefore, preventive action should be focussed on young women with low parity.
Cytotoxicity of inorganic mercury to the liver of two species, Anabas testudineus and Sprague Dawley male rat was evaluated. Distribution kinetics of this metal in the different hepatic subcellular fractions were followed for 48 h after a single injection of [203Hg] mercuric nitrate at a dose of 4mg/kg b.w. Interaction of this metal with protein, DNA and RNA was also studied. In rat, nuclear and lysosomal fractions showed a significant increase in the protein content, while in fish, the amount of protein increased in all fractions except microsome. Comparatively more mercury was bound to protein in fish during the later phase of treatment. Retention of mercury in nuclear DNA of rat gradually declined from 15 min to 48 h of treatment, while, mitochondrial DNA binding to mercury increased from 15 min to 2 h of post injection and then declined in the later phase of the experiment. Such a biphasic binding pattern of mercury was shown by both the nuclear and mitochondrial DNA of the fish. The nuclear RNA of rat and mitochondrial and cytosolic RNA of both test species also showed a biphasic pattern of mercury binding, however, with a higher rate of binding in fish at the later phase of the experiment. The present study thus highlights that (a) mercury follows a definite distribution pattern in the subcellular fractions of the liver in both animal species, (b) cytosol is the major site of mercury accumulation.
The distribution of mercury, an environmentally important toxicant, has been evaluated in a time dependent manner in different tissues of white rat and a freshwater teleost, Anabas testudineus. Sampling was performed at 15 min, 2, 6 and 48 h post injection (im) of 203Hg mercuric nitrate. Radioactivity of the 5% tissue homogenate, serum and bile was measured in a Gamma Counter. The rate of 203Hg accumulation is higher in fish immediately after administration which, however, is more or less of equal rate in the later period of observation in both the experimental animals. Partitioning of 203Hg occurs in a species specific manner with higher levels recorded in the brain and gonad of white rat. Spleen, liver and kidney, however, are the major tissues to accumulate mercury in both the species. The present study highlights that kidney is the target site of mercury retention with a higher kidney/liver ratio of mercury.
Twenty cases of eating epilepsy have been studied over a period of 5 years (1985-1989). Males outnumbered females (4:1). Heavy meal comprising conventional Indian diet (viz, rice, vegetables, etc), was found to be the most important provocating factor (14 out of 20 cases). The attacks occurred at lunch time in most cases (15). Thirteen cases had generalised seizures. Electro-encephalogram showed focal changes in 10 cases, generalised changes in 6 cases, while 4 cases had normal electro-encephalogram. Computerised tomography scan was normal in all the cases (7) when it was done.
The influence of triiodothyronine (T3) on the level of tubulin and other proteins in primary cultures of neuronal (N) and glial (G) cells from rat brain has been investigated. Quantitation of tubulin by [3H]colchicine binding assay revealed that when cells from 1 day rat brain were cultured for 18 hr with physiological doses (0.5-5 nM) of T3, the hormone elicited 35-40% increase in the soluble (30,000 g supernatant) tubulin content of G cells only. This stimulation was age-dependent and occurred neonatally at a time corresponding to the onset of synaptogenesis. In mouse and chick brain also, [3H]colchicine binding assay showed a similar selective stimulation of the soluble tubulin content of G cells by T3 with virtually no effect on N cells. However, SDS-polyacrylamide gel electrophoresis of the total proteins in the 30,000 g supernatants from N and C cells of rat brain, labeled for 18 hr with [14C]leucine in the presence of T3, revealed that T3 elicited 2-3-fold enhancement of radiolabeled tubulin in the N cells which is relatively greater than the 1.5-fold increase seen in the G cells. Analysis of the autoradiograms of these labeled proteins also revealed that in addition to tubulin, T3 stimulated the accumulation of radiolabeled actin by 1.5- and 2-fold in N cells and G cells respectively. Similar electrophoretic analysis of the solubilized labeled proteins in the 30,000 g pellets from N and G cells indicated that the failure to detect the stimulation of tubulin in the 30,000 g supernatants from N cells by [3H]colchicine binding assay could be at least partly due to rapid translocation of the dimeric soluble tubulin into insoluble membrane fractions or due to presence of higher oligomeric forms of tubulin which are insensitive to [3H]colchicine binding assay.
Previous work has established marked amplification of CCl4 hepatotoxicity by prior exposure to chlordecone (CD). Since CCl4 is toxic by virtue of its bioactivation by the hepatomicrosomal cytochrome P-450 (cyt P-450) system, which is in turn destroyed, our first interest was to determine if cyt P-450 isozymes were selectively destroyed in this interaction. CoCl2 also decreased hepatic P-450 contents, so our other interest was to observe whether CoCl2 selectively decreased or spared CCl4 metabolizing P-450 enzymes. Solubilized hepatic microsomes from variously treated rats were used. The treatment protocol was dietary CD (10 ppm, for 15 d), and CCl4 (100 microliters/kg, ip). The treatments were CD alone, CCl4 alone, CD + CCl4 and with or without CoCl2 (60 mg/kg/d, sc for 2 d) treatment on d 13 and 14 of the dietary protocol. The control group received normal diet and corn oil vehicle. The key mixed-function oxidase (MFO) parameters measured were microsomal protein, cyt P-450 content, and aminopyrine demethylase (APD). Decrease of P-450 levels ranged from 2.2-fold (CD + CCl4) to 1.3-fold (CD + CoCl2). APD activity decreased by 48 and 26.6% in CD + CCl4 and CD + CoCl2 treatments, respectively. Using an anion-exchange high-performance liquid chromatography (HPLC) column, solubilized microsomal hemoproteins were resolved into five peaks. The P-450 content associated with each peak was determined. In CD rats there was slight increase in peak heights, whereas peak heights in CCl4 and control treatments were similar. CoCl2 decreased all peaks, the decrease of peak I being maximal. In CD + CCl4 treatment, absence of peaks II and III was noted. Microsomal proteins stained for heme showed decreased staining intensity of hemo-protein bands, particularly band 4 (MW 52,000), which was absent in CD + CCl4 interaction. These findings suggest that (1) CoCl2 does not selectively decrease or spare any P-450 isozymes and (2) CD + CCl4 interaction does destroy specific P-450 isozymes.
Female Aedes aegypti which took partial blood meals from the skin lesions of untreated lepromatous leprosy (LL) patients were then allowed to continue feeding on 72-96-hr-old Swiss albino suckling mice (Rockefeller strain). The bitten portion of skin was removed, divided into two parts and processed for the extraction of bacilli by two different methods using chloroform and petroleum ether. The proboscis of some of the fed mosquitoes was dissected out and examined for viable bacilli (stained by fluorescein diacetate and ethidium bromide) and acid-fast bacilli (AFB). Out of 50 probosces dissected 45 were found positive for AFB, with bacillary counts ranging up to 246 (average 40.20 +/- SD 41.80) per proboscis. The average percentage of viable bacilli (green solid) in the probosces immediately after feeding on LL patients was 43.90 and thereafter it decreased gradually to 3 on the seventh day. In the petroleum ether extract of mouse skin viable bacilli were observed in numbers up to 37 (average 15.25 +/- SD 10.25) per smear. The number of fluorescing bacilli (green and red) correlated with the total number of AFB.
Batches of hungry Aedes aegypti mosquitoes which partially sucked blood from the skin lesions of proved untreated lepromatous leprosy (LL) patients were allowed immediately to feed on a portion of the skin of a cleanly shaved swiss mouse. The portion of the skin was cut, homogenized on the same day and extracted with chloroform. Out of 10 extracts, stained for acid fast bacilli (AFB), Mycobacterium leprae were demonstrated in eight, indicating transfer of bacilli mechanically to the biting spot through intermittent feeding. Out of 50 probosces dissected and stained for AFB, M. leprae were demonstrated in 45.
In vitro addition of some representative aliphatic, aromatic or heterocyclic compounds present in petroleum crude oils to washed rat platelets resulted in a concentration-dependent inhibition of aggregation induced by ADP or thrombin. Increasing concentration of extracellular Ca2+ did not alter the pattern of inhibition. ADP-induced intracellular Ca2+ mobilization was unaffected by most of the compounds tested. However, Ca2+ uptake was significantly inhibited when platelets were preincubated with these agents. This suggests that some components of crude oil may inhibit platelet aggregation by bringing about alterations in the platelet plasma membrane.
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Washed platelets isolated from rats 24 hr after oral treatment with a Prudhoe Bay crude oil (PBCO) showed a substantial inhibition of aggregation induced by ADP, arachidonic acid, or epinephrine. In vitro addition of a dimethyl sulfoxide extract of PBCO or its aliphatic, aromatic, or heterocyclic fractions to washed platelets also resulted in an inhibition of aggregation. ADP release was inhibited in platelets to which an extract of PBCO or its fractions were added in vitro or in platelets isolated from rats treated in vivo with PBCO. Thromboxane B2 release was increased in platelets isolated from rats intubated with PBCO or in platelets to which a dimethyl sulfoxide extract of the aromatic or heterocyclic fraction was added. However, thromboxane B2 release was inhibited in platelets to which PBCO or the aliphatic fraction extracts were added. The results indicate that PBCO inhibits platelet aggregation presumably by bringing about alterations in the platelet plasma membrane. Inhibition of ADP release could contribute to the inhibition of aggregation but thromboxane B2 is believed not to play a significant role.
Administration of a Prudhoe Bay crude oil (PBCO) to rats has been shown to (a) inhibit platelet aggregation induced by adenosine diphosphate (ADP), arachidonic acid, or epinephrine and (b) induce benzo-alpha-pyrene hydroxylase (BPH) in the liver and small intestine. Maximum inhibition of aggregation (90%) was seen 12 to 16 hours subsequent to dosing. However, substantial inhibition was observed as early as four hours and as late as 48 hours after dosing. Of particular interest was the sensitivity of the platelet response compared with the putatively sensitive response of monooxygenase induction in liver. As little as 0.1 ml of PBCO per kilogram body weight (bw) caused an inhibition of aggregation with all three agonists. A similar inhibition of the release of ADP from platelets in the presence of arachidonic acid or epinephrine was also observed. In contrast, hepatic BPH activity showed only a modest increase (67%) over the control value even after administration of 2 ml of PBCO per kilogram body weight. Small intestine BPH activity was more sensitive, showing a gradual increase of up to 19-fold 24 hours after dosing with 2 ml of PBCO per kilogram body weight. The sensitivity of the platelet response is of general environmental interest and evaluating platelet aggregation in humans may be important as a noninvasive assay for exposure to either accidental or "acceptable" levels of petroleum hydrocarbons in the occupational environment.
The effects of thyroid hormone on Na,K-ATPase alpha-subunit mRNA (mRNA alpha) content and Na,K-ATPase activity were measured in renal cortex, heart, and cerebrum of hypothyroid rats 24 and 72 h after injection of diluent or T3. Use of a cDNA probe complementary to rat brain mRNA alpha in Northern blot analysis revealed a single 26-27 S band in RNA isolated from these three tissues regardless of thyroid status. Tissue mRNA alpha content was estimated by dot blot analysis of whole cell extracts and isolated total RNA. Injection of T3 augmented mRNA alpha content by 2.1- to 2.5-fold in kidney cortex and myocardium at 24 h. After three daily injections of T3, the increases in mRNA alpha were evident despite a global increase in RNA content associated with hypertrophy of these target tissues. Furthermore, the increases in abundance of mRNA alpha after 72 h of T3 treatment correlated with enhancement of Na,K-ATPase activity. In contrast, both mRNA alpha and enzyme activity were invariant in the cerebrum. These data suggest that T3-induced augmentation of Na,K-ATPase activity is mediated, at least in part, by increased mRNA alpha content in target tissues.
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