Attenuation of Iron-Nitrilotriacetate(Fe-NTA)-mediated Renal Oxidative Stress, Toxicity and Hyperproliferative Response by the Prophylactic Treatment of Rats with Garlic Oil

Iqbal, Muzaffar; Athar, Mohammad

doi:10.1016/s0278-6915(98)00008-8

Cited by 99 publications

(57 citation statements)

References 33 publications

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“…Glutathione reductase activity was assayed by the method of Carlberg & Mannervik (1975), as modified by Iqbal et al (1998b). The assay system consisted of 1.7 ml phosphate buffer (0.1 M, pH 7.6), 0.1 ml EDTA (0.5 mM), 0.05 ml oxidized glutathione (1.0 mM), 0.1 ml NADPH (0.1 mM), 0.05 ml renal and hepatic PMS (10% w/v) in a total volume of 2.0 ml.…”

Section: Methodsmentioning

confidence: 99%

Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

Iqbal

Sharma

Okazaki

et al. 2003

Pharmacology & Toxicology

270

147

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Dietary antioxidants protect laboratory animals against the induction of tumours by a variety of chemical carcinogens. Among possible mechanism of protection against chemical carcinogenesis could be mediated via-antioxidantdependent induction of detoxifying enzymes. Curcumin, a yellow pigment from Curcuma longa, is a major component of turmeric and is commonly used as a spice and food colouring material and exhibits antiinflammatory, antitumour, and antioxidant properties. In this study we therefore investigated the effect of dietary supplementation of curcumin on the activities of antioxidant and phase II-metabolizing enzymes involved in detoxification, and production of reactive oxygen species were quantified in ddY male mice. Dietary supplementation of curcumin (2%, w/v) to male ddY mice for 30 days significantly increased the activities of glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase and catalase to 189%, 179%, 189%, and 181% in liver and 143%, 134%, 167% and 115% in kidney respectively as compared with corresponding normal diet fed control (PϽ0.05-0.001). Parallel to these changes, curcumin feeding to mice also resulted in a considerable enhancement in the activity of phase II-metabolizing enzymes viz. glutathione S-transferase and quinone reductase to 1.7 and 1.8 times in liver and 1.1 and 1.3 times in kidney respectively as compared with corresponding normal diet fed control (PϽ0.05-0.01). In general, the increase in activities of antioxidant and phase II-metabolizing enzymes was more pronounced in liver as compared to kidney. The induction of such detoxifying enzymes by curcumin suggest the potential value of this compound as protective agent against chemical carcinogenesis and other forms of electrophilic toxicity. The significance of these results can be implicated in relation to cancer chemopreventive effects of curcumin against the induction of tumours in various target organs.

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Section: Methodsmentioning

confidence: 99%

Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

Iqbal

Sharma

Okazaki

et al. 2003

Pharmacology & Toxicology

270

147

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“…19) Erythrocyte sedimentation rate (ESR) and clotting time (CT) 20) were also determined in the fresh blood of control and lithium nitrate treated animals. Serum was used for the blood urea nitrogen 21) and enzymological estimations.…”

Section: Chemicalsmentioning

confidence: 99%

Lithium Induced Toxicity in Rats: A Hematological, Biochemical and Histopathological Study

Sharma

Iqbal

2005

Biological & Pharmaceutical Bulletin

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The effect of long-term lithium treatment on renal function has been a matter of concern for about a quarter of centaury and remains controversial. For the last five decades researchers have been paying much attention to the lithium salts due to their therapeutic uses in controlling a variety of neurotic and psychosomatic manic depressions, neurotoxicity, affecting muricidal behavior and lithium sickness. [1][2][3][4] Extensive usage of lithium and its compounds in pharmaceuticals, dehumidifying and air conditioning units, ceramics and metallurgical processes, lubricants and in a number of chemical and biological laboratories brings this lightest alkali metal in close contact of human.Toxicity of lithium may be caused while taken as medicine. 5,6) Lithium salts cause ocular side effects, 7) polyuria, polydipsia, loss of body mass 8) and impaired renal concentration capacity after water deprivation.9) Lithium salts used as medicine can readily cross the placental barriers and produce teratogenic effects and toxicity. 10) In early pregnancy, lithium salt therapy elicited to be associated with a several fold increase in the incidence of cardiovascular anomalies in newborn, including tricuspid valve abnormalities.11) Cerebellar atropic changes related to lithium therapy 12) and peri-follicular inflammation and follicular plugging 13) even with the therapeutic limit of lithium level of blood have been observed. The occurrences of choreoathetosis 14) and abnormalities in lung and respiratory tract have also been reported by intake of lithium.15) Hypochromic microcytic anemia, hypercholesterolaemia, hyperglycemia, glycogenolysis, disturbance in TCA cycle and stimulation in transamination reaction in liver and kidney following repeated intramuscular injections of lithium nitrate in laboratory animals have been reported previously. 16,17) Renal insufficiency in long term lithium treatment has also been reported recently.18) This is an endeavor to study the histopathological and biochemical impacts of intake of small doses of lithium nitrate on renal tissue along with some blood parameters in male albino rats. Our results suggest that small doses of lithium induces toxicity in rats and therefore, studies evaluating its long-term tolerability are important. MATERIALS AND METHODS ChemicalsLithium nitrate, sodium citrate, diethylbarbiturate, 3,5-dinitrosalicilate, ammonium molybdate, citric acid, diacetylmonoxime, b sodium glycero phosphate, a ketoglutarate, a L-alaline, L-aspartate, sodium hypochlorite, trichloroacetic acid, and dinitrophenyl hydrazine were purchased from Sigma Chemical Company (St Louis, MO, U.S.A.). All other chemicals and reagent used were either of analytical grade or of highest purity, commercially available.Animals and Treatments Animals experiments were approved by animal care committee of Jamia Hamdard, care and handling of animals were in accordance with Indian Council of Medical Research guidelines. Male albino wistar rats (4-6 weeks) weighing 125-150 g, from Jamia Hamdard Central Animal House Col...

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“…Catalase activity, protein and/or mRNA levels have been found to be increased, [31][32][33] unchanged 34) or decreased [35][36][37][38][39][40][41][42] during oxidative stress. A ROS-mediated, biphasic model of catalase regulation has, however, been proposed in which catalase is stimulated by c-Abl/Arg-mediated phosphorylation at lower ROS levels, 43) while in the event of uncontrollable ROS levels, catalase is degraded by ubiquitinmediated proteasomal proteolysis, which thereby induces cell death.…”

Section: Discussionmentioning

confidence: 99%

Involvement of c-Met- and Phosphatidylinositol 3-Kinase Dependent Pathways in Arsenite-Induced Downregulation of Catalase in Hepatoma Cells

Kim

Lee

Kang

et al. 2011

Biological & Pharmaceutical Bulletin

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Cellular defense systems, including a variety of antioxidant molecules and enzymes such as superoxide dismutase, glutathione peroxidase and catalase, ensure that reactive oxygen species (ROS) are maintained at relatively low levels in normal conditions. 1) Arsenic and its compounds are welldocumented environmental toxicants 2) that induce oxidative damage by increasing the production of ROS. Oxidative damage has been suggested to play a key role in arsenicinduced toxicity. 3-7)Catalase protects cells from ROS-induced damage by catalyzing the breakdown of hydrogen peroxide (H 2 O 2 ) into oxygen and water. Arsenic has been demonstrated to decrease catalase expression both in animal tissues and cultured cells. Catalase activity is significantly decreased in the liver of rats treated with arsenite. [8][9][10] Arsenite treatment in vitro decreases catalase activity in human fibroblasts. 4) In a human keratinocyte cell line, it was also shown to decrease levels of catalase mRNA and protein. 11)Phosphatidylinositol 3-kinases (PI3Ks) are key components for the activation of Akt signaling. In the PI3K/Akt pathway, formation of 3-phosphoinositides by PI3K enables the activation of Akt by phosphoinositide-dependent protein kinases 1 and 2, which phosphorylate Akt at threonine residue 308 (Thr308) and serine residue 473 (Ser473), respectively. PI3K/Akt is thought to play a pivotal role in regulating cell proliferation, survival, metabolism and cancer progression. The PI3K/Akt pathway is downstream of c-Met receptor tyrosine kinase, a receptor for hepatocyte growth factor. [12][13][14] In c-Met-deficient mouse hepatocytes, the level of catalase protein is constitutively high, 15) suggesting that a cMet-dependent pathway is involved in catalase expression. Rat liver epithelial cells transformed by chronic exposure to arsenite show upregulated c-Met expression. Previous studies have demonstrated arsenite-induced activation of PI3K and c-Met-and PI3K-dependent inhibition of catalase expression. The aim of this study was to examine the involvement of c-Met-and PI3K-dependent pathways in arsenite-induced inhibition of catalase expression. Catalase mRNA and protein expression have been analyzed in human hepatoma cells treated with sodium arsenite and an inhibitor of either c-Met or PI3K. MATERIALS AND METHODS ChemicalsAll chemicals used were of reagent grade or higher and were obtained from Sigma-Aldrich (St. Louis, MO, U.S.A.), unless otherwise specified.Cell Treatment Human hepatoma cell line HepG2 was Seoul 156-756, Korea. Received July 13, 2011; accepted August 10, 2011; published

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Attenuation of Iron-Nitrilotriacetate(Fe-NTA)-mediated Renal Oxidative Stress, Toxicity and Hyperproliferative Response by the Prophylactic Treatment of Rats with Garlic Oil

Cited by 99 publications

References 33 publications

Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

Lithium Induced Toxicity in Rats: A Hematological, Biochemical and Histopathological Study

Involvement of c-Met- and Phosphatidylinositol 3-Kinase Dependent Pathways in Arsenite-Induced Downregulation of Catalase in Hepatoma Cells

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