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Biomedical subjects

G D Nadkarni

Publications and source records attributed to G D Nadkarni.

At least 19 recordsLinked to original sources
PubMed1999

Preparation and evaluation of liposomal formulations of tropicamide for ocular delivery.

Tropicamide, a mydriatic, cycloplegic drug was entrapped in liposomes. Liposomes were investigated by laser counting studies, transmission electron microscopy and differential scanning calorimetry for characterization. The precorneal clearance of liposomes was compared with solution by gamma-scintigraphy in the rabbit. The neutral liposomes failed to demonstrate significant enhancement in precorneal retention in comparison with aqueous solution. The potential of liposomes as an ophthalmic drug delivery system was investigated by comparing pupil dilatory effect of tropicamide by topical instillation, in the rabbit eye, of the solution and various drug-loaded liposomal forms, i.e. neutral liposomes, positively charged liposomes and neutral liposomes dispersed in 0.25% (w/v) polycarbophil gel. The positively charged liposomal formulation and liposomes dispersed in polycarbophil gel were found to be more effective than neutral liposomal dispersion when data were statistically treated at the 5% level of significance.

Animals↗
PubMed1998

Role of antioxidant defence in renal pathophysiology: primacy of glutathione peroxidase.

Antioxidant defences consisting of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and non-protein thiol (GSH) were estimated in the surviving kidney of unilaterally nephrectomized rats on days 1, 2, 3 and 12, following surgery. Simultaneously renal tissue lipid peroxidation (LP) and plasma GPx was monitored. The aim of this study was to evaluate the role of antioxidant defence in renal pathophysiology. Significant elevations in renal LP, GPx and GSH were evident on the first day and were maintained till 3rd day following nephrectomy. The response of SOD and catalase was slower, attaining significant elevation on 2nd and 3rd day respectively. Tissue GPx was the only parameter which remained elevated till 12th day, while all the other parameters returned to control levels by day 12. Plasma GPx declined significantly on days 3 (13.2%) and 12 (19.6%). These changes appear to be a part of the process when functions of 2 kidneys are taken over by a single kidney following unilateral nephrectomy.

Animals↗
PubMed1997

Changes in lipid peroxide levels and the activity of reactive oxygen scavenging systems in thyroid tissue after exposure to radioactive iodine in rats.

Exposure to ionizing radiation causes radiolysis of water in tissues leading to generation of reactive oxygen species (ROS), which are known to affect the antioxidant defense systems and induce lipid peroxidation (LP). Use of radioactive iodine (131I) for diagnosis and therapy of thyroid disorders may also generate ROS in the thyroid. Early (24 and 48 hours) and late (18 days) effects of subablation doses of 131I (370/555/1110 kBq) on the antioxidant defense and LP in the thyroid tissues have been studied. LP was elevated in all 131I treated groups by 10% to 41%. Although there was no change in catalase (CAT), the superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities showed evidence of change from 48 hours onwards--SOD decreased by 32% to 56% and GPx increased by 15% to 43%. Nonprotein thiols (reduced glutathione, GSH) showed an elevation of 16% at 24 hours, but later declined by 15% by day 18 after 370 KBq of 131I. Thus, the increase in LP observed may be due to beta irradiation induced ROS by 131I. The parallel decrease in SOD could be due to inactivation by ROS. The increase in GPx may be a consequence of induction due to elevated LP and/or ROS, which may be inadequate to lower the LP. In spite of elevated LP, the thyroid function appears to be normal.

Animals↗
PubMed1997

Reactive oxygen species involvement in ricin-induced thyroid toxicity in rat.

Ricin is known to have diverse effects on the cells of different organs like liver, kidney, pancreas, intestines and parathyroid. Acute decrease in serum thyroid hormone level 24 h after ricin administration (1.5 micrograms/100 g) led us to suspect the toxic action of ricin on the thyroid. We monitored the lipid peroxidation (LP) and anti-oxidant status of the thyroid tissue to determine the role, if any, played by reactive oxygen species (ROS) in this pathology. An increase of 39% in LP and 47% in superoxide dismutase, along with a 8.5% decrease in catalase points to the imbalance in the antioxidant defence involving hydrogen peroxide and its univalent reduction product, the hydroxyl radical. Thyroid histopathology shows destruction of thyroid follicles and necrosis, which may be due to ROS and may partly explain the 50% reduction in circulating thyroid hormones seen after ricin administration.

Animals↗
PubMed1996

Role of tissue antioxidant defence in thyroid cancers.

Reactive oxygen species (ROS), consisting mainly of superoxide, hydrogen peroxide and hydroxyl radical, have been implicated in many diseases including cancer. ROS have been known to play an important role in the initiation and promotion of multistage carcinogenesis. The cellular antioxidant defence plays a crucial role in neoplastic disease. However, very little is known about the tissue antioxidant defence in thyroid cancers. We therefore undertook a study to assess the role of ROS in the pathogenesis of thyroid cancers. Our samples consisted of post-operated thyroid tissues (normal, goiters, follicular adenomas, follicular carcinomas and papillary carcinomas). The parameters studied were lipid peroxidation (LP), antioxidant enzymes--superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)--and non-protein thiols (GSH). Compared to normal thyroid no changes were seen in goiters. LP was significantly higher in adenomas (16%) and carcinomas (60-69%). SOD was decreased by 15% in adenomas while in carcinomas it increased by 9-12%. GPx was raised in carcinomas by 10-21%. Follicular carcinomas showed a 4% increase in CAT activity while GSH was raised in adenomas and papillary carcinomas by 17%. Thus, in adenomas (initial stage) involvement of superoxide radicals and in carcinomas (later stage) hydrogen peroxide and, possibly, hydroxyl radical involvement cannot be ruled out. These ROS may be responsible for elevated LP observed in adenomas and carcinomas.

Adenoma↗
PubMed1994

Role of antioxidant enzyme defence in sparing rat hepatocytes from toxicity of ricin at low dose.

Ricin, a glycoprotein from castor oil seeds, is specifically toxic to Kupffer cells and at low doses it leaves parenchymal cells comparatively unaffected. At a dose of approximately 1.5 microgram/100 g body weight, ricin significantly increases the hepatic antioxidant enzyme system in rats within 24 hr. Superoxide dismutase, catalase and glutathione peroxidase show an increase in liver tissue levels of 19-24%. However, hepatic lipid peroxidation is elevated by about 34% and non-protein sulphydryl is reduced by 26%. The enhanced levels of antioxidant enzymes appear to protect the hepatocytes from the toxin. The observed elevation of hepatic thiobarbituric acid-reactive substances appears to originate mainly from the damaged Kupffer cells.

Animals↗
PubMed1993

Serum ferritin in thyroid cancer.

Serum ferritin, one of the nonspecific tumor markers, was studied in 102 thyroid cancer patients, who had been thyroidectomized and were off thyroxine for 1 month, making them hypothyroid. Serum ferritin in thyroid cancer patients was not significantly different as compared to controls. Nevertheless, high levels of serum ferritin were observed in the thyroid cancer group as compared to primary hypothyroid patients. Furthermore, there was a significant difference in serum ferritin between thyroid cancer patients without metastasis and those with metastasis, patients with metastasis showing higher levels. Classification of thyroid cancer patients into different histological types revealed higher ferritin levels in follicular carcinoma as compared to papillary carcinoma. These data suggest that, although serum ferritin may not be a tumor marker for thyroid cancer, this parameter seems to be sensitive to the presence of metastasis and the histologic diagnosis.

Adenocarcinoma, Follicular↗
PubMed1993

The role of calcium in the modulation of the hepatic anti-oxidant defence system.

A normocalcemic animal model of vitamin D (vit. D)-deficiency has been successfully developed by feeding a high calcium (Ca2+) diet to vit. D.-deficient rats. The modulating role of Ca2+ on the hepatic antioxidant defence system and lipid peroxidation has been evaluated in this model. Partial restoration of liver function was noted in these rats following extra Ca2+ feeding. Serum alkaline phosphatase and alanine aminotransferase reverted to a normal level. The reduced levels of hepatic SOD and glutathione peroxidase in vit. D.-deficient rats, were also increased after extra Ca2+ supplementation. Even elevated lipid peroxidation due to vit. D.-deficiency was reduced after feeding the extra Ca(2+)-supplemented diet. However, catalase activity remained at the control level throughout the study. The results provide important evidence that normocalcemia is essential for maintaining the hepatic antioxidant defence and controlling lipid peroxidation in the in vivo milieu.

Alkaline Phosphatase↗
PubMed1992

Relation between thyroid status and ferritin metabolism in rats.

Rats were made hypo and 'hyperthyroid' with propylthiouracil (PTU) and L-Thyroxine (L-T) respectively. The hypo and hyperthyroid status in these rats were confirmed by serum level of T4 and T3. Liver iron was significantly increased in both the hypo and hyperthyroid animals. However, liver ferritin synthesis rate was reduced by 36% in hypothyroid rats, and elevated by 38% in hyperthyroid ones. A similar trend was seen in liver ferritin concentration. Further, serum transaminases were elevated only in animals of the hyperthyroid group. It appears from the present data that ferritin metabolism is influenced by thyroid hormone as well as by iron. Thus, the raised serum ferritin in hyperthyroid patients may be partially attributed to increased ferritin synthesis in the liver and its possible leakage into circulation.

Albumins↗
PubMed1991

Effect of ricin on acute phase response in rats.

Ricin, a highly toxic protein from castor beans was administered (ip) to rats in a dose of 1.25 micrograms/100 g to selectively deplete at least 60-70% of Kupffer cells. This dose spared hepatocytes. This rat model was used to study acute phase protein synthesis and the role of Kupffer cells in acute phase response (APR). Ricin itself induced an APR, similar in pattern but of lower magnitude, than that induced by turpentine. However, the effect of combination of ricin and turpentine on APR was not additive. Kupffer cells appear to play permissive role in APR through mediators like hepatocytes stimulating factors.

Acute-Phase Proteins↗
PubMed1991

Biokinetics of 99mTc-labelled liver-imaging agents in an animal model of liver cirrhosis.

Comparable degree of liver cirrhosis, as judged by liver function tests and histopathology, was induced in rats by carbon tetrachloride. Comparative organ distribution of 99mTc-sulphur colloid and 99mTc-phytate was studied in the liver, spleen and lungs of these cirrhotic rats. Compared to controls, the biodistribution of 99mTc-sulphur colloid was found to be affected more than that of 99mTc-phytate in cirrhotic rats, especially at early time intervals.

Animals↗
PubMed1990

Plasma orosomucoid metabolism and susceptibility to malarial infection in rodents.

The effects of Plasmodium berghei infection on liver function and plasma orosomucoid metabolism were investigated in Wistar rats. Infected rats with 20-25% parasitaemia manifested increased serum transaminase levels, hypoalbuminaemia and hypoproteinaemia. In spite of such indications of deranged liver function, the hepatic synthesis rate (as measured by 14C-amino acid incorporation) of seromucoids predominantly orosomucoid or alpha 1-acid glycoprotein) was increased by 73%. The circulating levels of this glycoprotein were also doubled in infected animals. The albumin synthesis rate was not increased. This preferential synthesis and increase in circulating levels of orosomucoid may have in vivo significance in malarial infection, in view of reports that orosomuocid has influence on in vitro invasion of red cells by malarial parasites.

Animals↗
PubMed1989

Altered hepatic function in vitamin D-deprived rats.

Rats were rendered vitamin D-deficient by housing them in a room free of ultraviolet light and maintaining them for 20 weeks on a diet devoid of only vitamin D. The vitamin D-deficiency state was confirmed by the undetectable levels of circulating vitamin D metabolites, severe hypocalcaemia and significantly reduced intestinal calcium transport. Liver function and protein metabolism in these rats were assessed by bromosulphthalein (BSP) clearance, liver histology, plasma transaminases and alkaline phosphatase, and 14C-labelled amino acid incorporation into liver and plasma proteins. Subtle alterations in hepatic function, as manifested by delayed BSP clearance, elevated levels of plasma transaminases and alkaline phosphatase, were noticed. Liver histology revealed changes consistent with periportal necrosis. Synthesis of liver and plasma proteins were reduced by 26-34% (P less than 0.01), without affecting the circulating levels of plasma proteins, suggesting reduced protein turnover in vitamin D-deprived rats. The results strongly suggest the direct/indirect involvement of vitamin D in mediating the altered liver function.

Animals↗
PubMed1989

Liver function and plasma protein metabolism in rodent model of filariasis.

Rodent model of filariasis was developed by infecting Wistar rats with Litomosoides carinii. Liver function tests, plasma protein concentrations, and synthesis rates of liver-formed proteins were estimated in these rats at 63 and 90 days post-infection. At 63 days post-infection, aspartate aminotransferase and alkaline phosphatase were significantly increased. Alanine aminotransferase, plasma total proteins and plasma albumin were in the normal range. However, at 90 days post-infection all these parameters were affected, reflecting progressive liver involvement. Hypoalbuminemia at 90 days post-infection did not appear to be due to decreased synthesis rate, indicating higher catabolism and/or altered distribution in pools.

Animals↗
PubMed1989

Quantitation of gastrointestinal protein loss.

Plasma proteins leak into the gastrointestinal tract under physiological conditions. This may assume enormous proportions in certain pathological conditions associated with the stomach, intestines, intestinal lymphatics and capillaries, resulting in severe hypoproteinemia. Quantitation of this leakage has been achieved by using plasma proteins or non-protein foreign colloids and macromolecules labelled with radioactive isotopes. The requirements of an ideal label have been listed and the advantages/disadvantages of different tracer labels have been reviewed. No label presently available fulfils all the requirements of an ideal tracer. In spite of this, a wealth of information has been acquired by gastroenterologists to unravel the mystery of hypoproteinemia of unknown cause.

Digestive System↗
PubMed1988

Antioxidant and free radical-scavenging enzymes in chronically ethanol-consuming rats: controversy over hepatic lipid peroxidation.

In rats given ethanol 20% (v/v) in drinking water the hepatic antioxidant enzymes, superoxide dismutase (SOD), catalase and glutathione peroxidase were assayed at the end of 4 and 10 months of ethanol consumption. Simultaneously hepatic lipid peroxidation was monitored. At 4 months SOD and catalase were unaffected, while glutathione peroxidase was decreased by 48%. By the end of 10 months SOD had declined by 16% and glutathione peroxidase activity increased by 49%, while catalase again remained stable. However, hepatic lipid peroxidation was not significantly affected throughout the study. The controversy in the literature over the conflicting results of hepatic lipid peroxidation in chronically ethanol-fed rats is discussed in the light of mode, dose, duration of ethanol consumption, nutritional status of the rat, and primacy of glutathione peroxidase.

Alcoholism↗
PubMed1988

Hepatic antioxidant enzymes and lipid peroxidation in carbon tetrachloride-induced liver cirrhosis in rats.

Liver cirrhosis was induced in rats by the combined action of oral phenobarbitone and inhalations of carbon tetrachloride vapors. These rats manifested hepatosplenomegaly, hypoalbuminemia, and 2- to 17-fold elevations in serum transaminases and alkaline phosphatase levels. The hepatic antioxidant enzymes, superoxide dismutase and catalase, showed 28 and 60% decreases, respectively. There was, however, no increase in the hepatic lipid peroxidation. These studies suggest that in cirrhosis liver cell damage may result due to the direct attack of the oxygen free radicals. Lipid peroxidation in the liver may not be a prerequisite for the development of cirrhosis, as is generally believed.

Animals↗