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Biomedical subjects

S B Lall

Publications and source records attributed to S B Lall.

At least 19 recordsLinked to original sources
PubMed2001

Cholinesterase inhibition by aluminium phosphide poisoning in rats and effects of atropine and pralidoxime chloride.

AIM: To investigate the cholinesterase inhibition and effect of atropine and pralidoxime (PAM) treatment on the survival time in the rat model of aluminium phosphide (AlP) poisoning. METHODS: The rats were treated with AlP (10 mg/kg; 5.55 x LD50; ig) and the survival time was noted. The effect of atropine (1 mg/kg, ip) and PAM (5 mg/kg, ip) was noted on the above. Atropine and PAM were administered 5 min after AlP. Plasma cholinesterase levels were measured spectrophotometrically in the control and AlP treated rats 30 min after administration. RESULTS: Treatment with atropine and PAM increased the survival time by 2.5 fold (1.4 h+/-0.3 h vs 3.4 h+/-2.5 h, P < 0.01) in 9 out of 15 animals and resulted in total survival of the 6 remaining animals. Plasma cholinesterase levels were inhibited by 47 %, (438+/-74) U/L in AlP treated rats as compared to control (840+/-90) U/L (P < 0.01). CONCLUSION: This preliminary study concludes that AlP poisoning causes cholinesterase inhibition and responds to treatment with atropine and PAM.

Aluminum Compounds↗
PubMed2001

Effect of N-acetylcysteine and L-NAME on aluminium phosphide induced cardiovascular toxicity in rats.

AIM: To investigate the protective effects of N-acetylcysteine (NAC) and Nomega-Nitro-L-arginine methyl ester (L-NAME) on aluminium phosphide (AlP) poisoning induced hemodynamic changes, myocardial oxygen free radical injury and on survival time in rats. METHODS: AlP (12.5 mg/kg) was administered intragastrically under urethane anaesthesia. The effect of pre- and post-treatment with NAC and L-NAME alone and in combination was studied on haemodynamic parameters [blood pressure (BP), heart rate (HR), and electrocardiogram (ECG)] and biochemical parameters (malonyldialdehyde, catalase, and glutathione peroxidase). RESULTS: AlP caused significant hypotension, tachycardia, ECG abnormalities, and finally marked bradycardia. The mean survival time was (90 +/- 10) min. There was significant increase in myocardial malonyldialdehyde (MDA), and decrease in catalase and glutathione peroxidase (GSH Px) levels. NAC infusion (6.25 mg . kg-1 . min-1, iv for 30 min) caused insignificant hemodynamic and biochemical changes. Pre- and post-treatment of NAC with AlP significantly increased the survival time, stabilized BP, HR, and ECG, decreased MDA and increased GSH Px levels compared to AlP group. L-NAME infusion (1 mg . kg-1 . min-1, iv for 60 min) as such caused significant rise in BP but precipitated ECG abnormalities. Pre- and post-treatment of L-NAME with AlP neither improved the survival time nor the biochemical parameters despite significant rise in BP. Co-administration of both the drugs with AlP worsened the hemodynamic and biochemical parameters with reduction in the survival time as compared to AlP. CONCLUSION: NAC increased the survival time by reducing myocardial oxidative injury whereas L-NAME showed no such protective effects in rats exposed to AlP.

Acetylcysteine↗
PubMed2000

Humoral and cell mediated immune response to cadmium in mice.

The effect of 30, 100 and 300 ppm of cadmium chloride (CdCl2) exposure for 35 days on humoral and cell mediated immune response was examined in Swiss Albino mice. Body burden of cadmium in kidney, spleen and liver was determined and histopathology of these organs was also done. Cadmium chloride in doses of 100 and 300 ppm when fed in drinking water caused significant decrease in IgM and IgG titre against sheep red blood cells (SRBC) and a significant decrease in IgG titre against bovine serum albumin (BSA). The delayed type hypersensitivity response to SRBC and splenic T cell proliferation to BSA was also significantly decreased following 100 amd 300 ppm cadmium exposure. Cadmium accumulation in the spleen, liver and kidney was associated with degeneration and inflammatory changes. It is concluded that cadmium causes significant suppression of humoral and cell mediated immune response in mice which could be due to its cytotoxic action on liver, kidney and immune cells.

Animals↗
PubMed2000

Effect of intra-tracheal instillation and inhalation of silicon dioxide on some biochemical variables in broncho-alveolar lavage fluid and lung histopathology in rats.

In the present study, the bronchial alveolar lavage fluid (BALF) biochemical and lung histopathological changes occurring in response to single large intra-tracheal exposure to silica have been compared to the changes seen after continued chronic exposure via inhalation. Male albino rats (200-250gms) were exposed to silicon dioxide via intratracheal instillation (8mg/0.05ml saline) and whole body inhalation (200mg/m3, 6 hours/day for 2 and 4 weeks) in separate groups . The respective control animals were instilled with normal saline (0.05ml) or exposed to fresh air in simulation chamber for the same duration. BALF was analyzed for total protein, elastase, malondialdehyde (MDA) levels and catalase activity and histopathology of right lung was carried out after 4 weeks post-exposure in intra-tracheal model and after 2 and 4 weeks of exposure in the inhalation model. The levels of total protein, elastase and malondialdehyde (MDA) were significantly elevated, while catalase activity was significantly decreased in the BALF of exposed animals as compared to controls. The histopathological studies of lungs, showed exudates of inflammatory cells, chiefly of macrophages in the alveolar spaces and interstitial septa with multifocal nodular granulomatous lesions. The biochemical findings in BALF of both the models indicate inflammatory changes, lipid peroxidation and fibrosis. However, comparatively lower catalase activity and higher elastase levels in the 4 week inhalationally exposed group than the 4 week post intratracheally exposed group, suggests that these parameters may be affected by acute and chronic exposure and require further confirmation.

Animals↗
PubMed2000

Pulmonary histopathology and alteration in cellular pattern of bronchoalveolar lavage fluid in experimental silicosis.

Pathogenesis of silicosis is still being evaluated. Cellular and histopathological changes in lung following acute and chronic exposure of quartz in rats have been investigated. Inbred wistar rats were given single intratracheal injection of quartz (10 mg in 0.05 ml saline) in groups of acute model, and inhalation of quartz (40 mg/m3 with air flow 5 l/hr in a simulation chamber, 6 hr/day) in groups of chronic model. The control groups were exposed to vehicles only. Rats were sacrificed on day 3, 5 and 7 of intratracheal injection and after 2, 4 and 8 weeks of inhalation. Total and differential cell counts (TC and DC) were performed in bronchoalveolar lavage fluid (BALF). Histopathology was done in the lungs. There was significant (P < 0.001) increase in TC and significant (P < 0.001) changes in percentage of inflammatory cell counts on DC in the BALF of silicotic rats. Histopathology showed progressive inflammatory and fibrotic response in quartz exposed lungs in both acute and chronic models. The results indicate duration dependent inflammatory changes in lungs of both the models. Changes in cell counts precede the histopathological changes and may serve as early biological marker for detection of silicosis.

Acute Disease↗
PubMed2000

Methemoglobinemia in aluminium phosphide poisoning in rats.

Aluminium phosphide (AlP) a grain fumigant is the leading cause of intentional poisoning in North India. The mechanisms involved in toxicity are not known and there is no antidote till date. The present study was carried out to investigate the oxygen free radical generation, methemoglobinemia and effect of methylene blue treatment on survival time in rat model of AlP poisoning. AlP (50 mg/kg, intragastric) was administered in one group and the other group received AlP + Methylene Blue (MB) (0.1%, 1 mg/kg/5 min, i.v.). Malonyldialdehyde (MDA) and methemoglobin (MeHb) levels were measured at 10 and 30 min intervals. Blood MDA levels increased at 10 and 30 min after AlP exposure with simultaneous rise in MeHb levels suggesting methemoglobinemia could be due to increased oxygen free radical generation. Methylene blue caused a significant fall in both the parameters with prolongation of survival time. It is concluded that AlP causes methemoglobinemia responding to methylene blue treatment.

Aluminum Compounds↗
PubMed1999

Role of corticosteroids in cadmium induced immunotoxicity.

Cadmium chloride at doses of 30, 100 and 300 ppm was orally fed to swiss albino mice for 35 days and the humoral and cell mediated immunity was studied by measuring the haemagglutination titre and delayed type hypersensitivity response respectively. Further, the blood corticosteroid level was determined in all the groups. Cadmium at doses of 100 and 300 ppm was found to significantly (p < 0.05) suppress both humoral and cellular immunity with simultaneous increase in the level of blood corticosterone and aldosterone. In order to assess whether the suppression of immune response in cadmium exposed mice is mediated by corticosteroids, aminoglutethemide, an adrenal blocker was administered to mice along with cadmium and the immune response was studied. Aminoglutethemide when administered alone caused significant (p < 0.05) stimulation of immunoglobulin level and delayed type hypersensitivity response as compared to cadmium (300 ppm) fed mice. When co-administered with cadmium, the cadmium induced immunosuppression was reversed back to normal. The results of this study indicate the involvement of adrenal hormones in cadmium induced immunosuppression suggesting that cadmium activates the corticosteroid associated immunoregulatory circuit.

Adjuvants, Immunologic↗
PubMed1999

Role of nutrition in toxic injury.

The importance of nutrition in protecting the living organism against the potentially lethal effects of reactive oxygen species and toxic environmental chemicals has recently been realized. This new perspective has prompted re-evaluation of the food constituents of human diet from the point of view of their nutritional adequacy, deficiency and toxicity. The biological antioxidant defense system is an integrated array of enzymes, antioxidants and free radical scavengers. These include glutathione reductase, glutathione-s-transferase, glutathione peroxidase, phospholipid hydroperoxide glutathione peroxidase, superoxide dismutase (SOD) and catalase, together with the antioxidant vitamins C, E and A. The individual components of this system get utilized in various physiological process and for chemoprotection and therefore require replenishment from the diet. Other components of the diet like carbohydrates, proteins and lipids are important for maintaining the levels of various enzymes required in body's defense system providing protection against carcinogens. However, the emerging newer concepts focus on the role of trace elements and other dietary components in antioxidant defense and detoxification mechanisms. Trace elements like Iron, zinc magnesium, selenium, copper, and manganese are some of the elements involved in antioxidant defense mechanisms. Inadequate intake of these nutrients has been associated with ischemic heart disease, arthritis, stroke and cancer, where pathogenic role of free radicals is suggested. Further the importance of diet in the prevention of chemical induced toxicity can not be undetermined. Recent reports on the role of bioflavonoids as antioxidents and their potential use to reduce the risks of coronary heart disease and cancer in human beings have opened a new arena for future research. Induction of the cytochrome P450 isoenzymes by food pyrolysis, mutagens, alcohol and fasting, on the other hand is reported to contribute to chemical toxicity and carcinogenecity. Certain chemicals moieties in the food are mutagenic and carcinogenic.

Animals↗
PubMed1998

Biochemical and histopathological changes in respiratory system of rats following exposure to diesel exhaust.

Effect of exposure to diesel exhaust (DE) for different durations was evaluated using histopathological and biochemical parameters in respiratory system of the rats. Animals were exposed to 1 part DE diluted with 5 parts of clean air in a simulation chamber for 15 min/day for 1, 7, 14 and 21 days. After completion of various exposures, biochemical parameters including elastase inhibitory capacity (EIC) and protein content of the bronchial airway lavage (BAL) and histopathological changes along with lung/body weight ratio were assessed. The elastase inhibitory capacity (an index of the protection against destruction of elastin, a lung connective tissue) was maximum at 1 week indicating thereby that the body renders protection against injury by increasing EIC levels in the initial phase. However, protein content in the BALF increased after 1 week and reached maximum at 2 weeks. Histopathological changes followed similar time course of pattern with accumulation of macrophages and protein exudation. Prolonged exposure up to 3 weeks, however was accompanied by chronic inflammatory changes and thickening of alveolar septa and blood vessels. Changes in lung/body weight ratio and suspended particulate matter (SPM) deposited on filters (simulation chamber) correlated well with EIC, protein content in BALF and histopathological changes. The biochemical findings accompanied with chronic structural changes in the lungs of rats following exposure to DE could be relevant to the clinical observation of increased incidence of chronic lung diseases after continued DE exposure.

Air Pollutants↗
PubMed1997

Cadmium induced nephrotoxicity in rats.

Onset of hypertension and nephropathy after 1,2, and 4 weeks of exposure to cadmium chloride (1 mg/kg, ip) was studied in rats by measuring changes in blood pressure and renal function (urinary output, electrolytes, serum creatinine, inulin clearance and Na+K+ ATPase). Significant decrease in body weight and rise in blood pressure were observed as early as one week of exposure while microalbuminuria was detected in 50% of the animals after 2 weeks. Na+K+ ATPase, a renal tubular enzyme, was depressed after 1 week with maximum lowering occurring after 4 weeks. There were no detectable changes in fluid intake, urine output, electrolytes, inulin clearance and serum creatinine even after 4 weeks. It is concluded that hypertension and tubular lesion set in earlier than glomerulopathy as indicated by microalbuminuria and the latter could be the consequence of rise in blood pressure.

Animals↗
PubMed1997

Involvement of renin-angiotensin system in hypertensive effect of cadmium in rats.

Role of renin-angiotensin system in hypertension induced by cadmium chloride (CdCl2) in rats has been investigated. Intravenous administration of CdCl (1 mg/kg) produced a biphasic response i.e. a transient fall followed by a marked and consistent rise in blood pressure. The peak hypertensive effect was accompanied by raised PRA levels. Pretreatment with captopril (1 mg/kg, i.v.) losartan (1 mg/kg, i.v.) or captopril + losartan attenuated the pressor response to Cd by 62%, 42% and 100% respectively in separate groups. Central administration of Cd (10 micrograms/rat, i.c.v.) showed a biphasic response similar to that observed after i.v. route. However, it was not accompanied by raised PRA levels. Prior treatment with losartan (10 micrograms/rat, i.c.v.) completely abolished the pressor response to Cd (i.c.v.) whereas it was not affected significantly by captopril (10 micrograms/rat, i.c.v.). On the other hand, centrally administered losartan only partially reduced the pressor response to i.v. Cd. The results are discussed in light of a differential involvement of central vs peripheral renin-angiotensin system in the hypertensive effect of Cd.

Animals↗
PubMed1997

An experimental study on cardiotoxicity of aluminium phosphide.

Aluminium phosphide(AlP), a grain fumigant pesticide, was studied for its cardiotoxicity in anaesthetised rats. The hemodynamic and cardiac biochemical changes were investigated following intragastric administration of different doses of AlP (10, 20 and 40 mg). With 10 and 20 mg dose of AlP an immediate fall in BP was observed which recovered partially and stabilized for 10 minutes followed by a gradual fall till the animal died. However, with a higher dose (40 mg) there was no recovery in BP, instead the initial fall continued till the death of the animal. An increase in the heart rate was observed with 10 and 20 mg dose of AlP for 15 minutes which was followed by a marked fall till cardiac arrest ensued. On the other hand, 40 mg dose produced only a transient tachycardia followed by a prolonged bradycardia. ECG changes at all dose levels included initial tachycardia and ST segment elevation progressing to QRS broadening. However, marked conduction defects as evidenced by the ventricular ectopics were noticed only with 40 mg. The mean survival time dose dependently decreased with 10 mg(55 +/- 3 min), 20 mg(35 +/- 2 min) and 40 mg(18 +/- 2 min) of AlP. The cardiac glycogen, ATP and CP levels were significantly lowered in animals treated with 10, 20 and 40 mg of AlP. Higher levels of MDA in the cardiac tissue were observed with 10, 20 and 40 mg of AlP. Thus it is suggested that the deleterious effect of AlP on heart is mediated by both declined cellular metabolism of the myocardium as well as by necrosis of the cardiac tissue resulting in the release of reactive oxygen intermediates.

Aluminum Compounds↗
PubMed1997

Effect of short and long-term exposure to diesel exhaust on sensitivity of guinea pig tracheal preparation to histamine.

Single exposure, to diesel exhaust (1 part exhaust diluted by 5 parts of clean air) reduced EC50 of histamine indicating hyperresponsiveness of the receptors in trachea of exposed guinea pigs. In contrast, following repeated exposure for 7, 14 or 21 days (15 min/day), EC50 was progressively increased indicating the possibility of down-regulated histamine receptors. Further, simultaneous significant increase in histamine levels (bioassayed on guinea pig ileum) in bronchial airway lavage fluid supports the aforementioned hypothesis. The change in lung/body weight ratio and suspended particulate matter deposited on filters followed the same temporal pattern as EC50. The findings are suggestive of differential effects of diesel exhaust on airway depending upon the duration of exposure.

Air Pollutants↗
PubMed1996

Angiotensin II--receptor subtypes characterization and pathophysiological implications.

In the past decade there have been considerable advances in basic knowledge of the renin-angiotensin system (RAS). The most important new development has been the appreciation of a tissue based RAS that can be independently regulated from the renal and vascular RAS. Greater insight into the mechanism by which angiotension-II (AII) exerts its action has been achieved through the study of molecular biology and pharmacological characterization of multiple receptor subtypes. This review summarises the features and distribution of several binding subtypes that may mediate the diverse functions of AII. Of these AT1 subtype is the most well known receptor which preferentially binds AII and AIII. The AT1 receptor site appears to mediate the classic angiotensin responses concerned with the body water balance and the maintenance of blood pressure. Less is known about the AT2 sites which also bind AII and AIII and may play a role in vascular growth. Recently, an AT3 has been discovered in cultured neuroblastoma cells and an AT4 site which preferentially binds AIV. It has been implicated in memory aquisition and retrieval and in the regulation of blood flow. Another important aspect covered is the primary and secondary messengers involved during the signal transduction after the binding of AII with receptors. A stress has also been given on the regulation of density and affinity of AII receptors by various physiological parametres as they affect the responses of RAS. Autoregulation by RAS, salt intake, development and aging and some of the hormones are important variables which could affect the AII receptors. Interactions of AII with various neuroeffector transmission involved in the regulation of water-electrolyte balance and BP regulation play an important role in the maintenance of the homeostasis. AII has been suggested to increase the NAergic transmission by enhancing synthesis, release, inhibiting reuptake by the presynaptic nerve terminals as well as enhancing cell responsiveness to the transmitter. The finding of existence of AII receptors in vagal afferent nerve terminals suggests that its baroreflex inhibitory effect is mediated by inhibiting neurotransmitter release at NTS in the baroreflex arc. Moreover, AII acts on the central receptors to stimulate AVP and ACTH secretion, drinking and peripherally increase synthesis and secretion of aldosterone. Interactions of RAS with kallikrein-kinin system and prostaglandins strongly support the existence of a balance between renal depressor and pressor substances. AII is now considered a growth promotor in cardiovascular tissues and the resultant vascular hypertrophy could contribute in the maintenance of hypertension. AII also plays a role in the kidney, not only as a regulator of hemodynamics but also in the structural changes occurring in a variety of renal disorders. In addition to the more well studied functions of RAS in RVH the review also highlights the potential contribution by the RAS to other clinically relevant syndromes such as aortoarterities induced RVH, hyperaldosteronism, heavy metal induced cardiovascular effects, diabetes mellitus and thyroid dysfunction. Although the receptor subtypes involved in these pathological states have not been definitely identified, research efforts in this direction are ongoing.

Animals↗
PubMed1995

Plasma renin activity in normal healthy volunteers: effect of physiological variables.

Plasma renin activity was determined in hundred normal subjects of either sex (M = 65, F = 35, age range 2-70 yr) using Angiotensin-I test kits. The effect of various physiological variables viz, age, sex, posture and salt intake was determined. The basal values for PRA ranged from 1.19 +/- 0.09 ng/ml/hr for males and 1.02 +/- 0.12 ng/ml/hr for females in erect posture. In contrast high basal supine PRA was noticed in subjects on low salt diet, which showed a significant increase in erect posture. A marked decrease in PRA with advancing age in both the sexes with significantly low values at higher age range was noticed. Captopril produced an insignificant effect on PRA and BP in salt replete supine state, whereas in salt deplete state there was a significant rise in both the parameters.

Adolescent↗
PubMed1995

Radioimmunoassay of angiotensin-II: methodology and standardization.

The study was planned to set up and standardize the radioimmunoassay of Ang-II and to validate the procedure in terms of precision, sensitivity, specificity and recovery. The application of the developed assay was studied in normal healthy volunteers and in patients of renovascular hypertension (RVHT) and renal hypertension (RH). Synthetic human Ang-II was coupled to BSA by carbodimide condensation to get the hapten carrier conjugate which was injected in rabbits to raise the antibodies. The titre of 1:250 showed significant binding (56.79%) and was used for the assay. The sensitivity of the assay was 2 pg/ml and cross-reactivity with analogues of Ang-II was minimum. Mean Ang-II levels in normal subjects was 16 +/- 3.6 pg/ml. In patients of RVHT and RH, the peripheral blood Ang-II levels were found to be 876 +/- 8.6 and 108 +/- 2.3 pg/ml respectively. In patients of unilateral RVHT, renal vein Ang-II levels of the affected side were significantly higher than the unaffected side (P < 0.001). The results indicate that unextracted samples can be successfully utilized to estimate Ang-II levels.

Adult↗
PubMed1994

Reduced urinary kallikrein excretion in human renovascular hypertension caused by nonspecific aortoarteritis and other disorders.

In this study urinary kallikrein excretion was measured using the kininogenase bioassay technique in 12 normal volunteers and 23 patients with angiographically-proven renovascular hypertension (RVHT). In 13 of these (group I), RVHT was due to nonspecific aortoarteritis (NSAA) and in 10 (group II) due to other causes. Urinary kallikrein (UKa) excretion was significantly lower in patients, with values still lower in NSAA. PRA was high in both the groups in comparison with controls; however, the levels were significantly lower in group I compared with group II. Finding of both UKa and PRA lower in group I is suggestive of long standing hypertension becoming volume dependent with nephrosclerotic changes in the kidney. These results point to decreased renal kallikrein-kinin system activity as a feature of NSAA that probably contributes chiefly to the maintenance of the hypertensive state. Normalisation of BP with restoration of UKa and PRA towards normal in three patients of group I and five in group II further support the role of UKa not only when over activity of renin-angiotensin system is responsible for RVHT as in group II but also in group I when the hypertension becomes volume dependent.

Adolescent↗