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1.
Article in English | IMSEAR | ID: sea-135645

ABSTRACT

Proper intake of dietary nutrients is considered crucial for preventing the initiation of events leading to the development of carcinoma. Many dietary compounds have been considered to contribute in cancer prevention including zinc, which plays a pivotal role in host defense against the initiation and promotion of several malignancies. Zinc is an essential element that is integral to many proteins and transcription factors which regulate key cellular functions such as the response to oxidative stress, DNA replication, DNA damage repair, cell cycle progression, and apoptosis. Zinc has been ascribed roles in the metabolism and interaction of malignant cells, particularly in apoptosis. Zinc is involved in structural stabilization and activation of the p53 that appears to be an important component of the apoptotic process and also in activation of certain members of the caspase family of proteases. Zinc exerts a positive beneficial effect against chemically induced preneoplastic progression in rats and provides an effective dietary chemopreventive approach to disease in vulnerable section of population with family history of carcinoma. The present review provides an insight into the research conducted on animals as well as on human subjects for providing the concept that zinc deficiency is an important factor in the development and progression of malignancy and that zinc could be efficacious in the prevention and treatment of several cancers viz., colon, pancreas, oesophageal and head and neck. However, it needs further exploration with regard to other definitive bioassays including protein expression and documentation of specific molecular markers to establish the exact mechanism for zinc-mediated cancer chemoprevention. Preclinical trials need to investigate the genetic and epigenetic pathways of chemoprevention by zinc.


Subject(s)
Animals , Apoptosis/physiology , Carcinoma/drug therapy , Carcinoma/prevention & control , Caspase 6/metabolism , Humans , Rats , Tumor Suppressor Protein p53/metabolism , Zinc/deficiency , Zinc/metabolism , Zinc/therapeutic use
2.
Indian J Exp Biol ; 2007 Nov; 45(11): 954-8
Article in English | IMSEAR | ID: sea-61330

ABSTRACT

With a view to find out whether zinc affords protection against lithium toxicity the activities of antioxidant enzymes and lipid peroxidation profile were determined in the cerebrum and cerebellum of lithium treated female Sprague Dawley rats. Lipid peroxidation was significantly increased in both the cerebrum and the cerebellum of animals administered with lithium for a total duration of 4 months as compared to the normal control group. On the contrary, the activities of catalase and glutathione-s-transferase (GST) were significantly reduced after 4 months of lithium treatment. The activity of superoxide dismutase (SOD) was significantly increased in the cerebrum after 4 months lithium administration, whereas in the cerebellum the enzyme activity was unaffected. No significant change in the levels of reduced glutathione (GSH) was found in either cerebrum or cerebellum after 2 months of lithium treatment. However, 4 months lithium treatment did produce significant changes in GSH levels in the cerebrum and in the cerebellum. Zinc supplementation for 4 months in lithium-treated rats significantly increased the activities of catalase and GST in the cerebellum, showing that the treatment with zinc reversed the lithium induced depression in these enzyme activities. Though, zinc treatment tended to normalize the SOD activity in the cerebrum yet it was still significantly higher in comparison to normal levels. From the present study, it can be concluded that the antiperoxidative property of zinc is effective in reversing the oxidative stress induced by lithium toxicity in the rat brain.


Subject(s)
Animals , Antidepressive Agents/adverse effects , Antioxidants/metabolism , Brain/drug effects , Cerebellum/drug effects , Cerebrum/drug effects , Female , Lipid Peroxidation/drug effects , Lithium Carbonate/adverse effects , Neuroprotective Agents/administration & dosage , Rats , Rats, Sprague-Dawley , Zinc Sulfate/administration & dosage
3.
Article in English | IMSEAR | ID: sea-114095

ABSTRACT

Chemical composition of the aerosols is an important aspect of aerosol monitoring. The adverse effects on human heath due to different elements in aerosols depend on their concentrations. A comparative study of aerosol concentration and composition from an industrial town Mandi-Gobindgarh and a nearby (25 km away) non-industrial and comparatively less polluted town Morinda, in state Punjab (India) was carried out. Aerosol samples were analyzed by Particle Induced X-ray Emission (PIXE) technique at the Institute of Physics, Bhubaneshwar. Elemental concentrations were found to be much higher in Mandi-Gobindgarh as compared to Morinda. However, the large deviations from the mean concentrations, particularly in Mandi-Gobindgarh is suggestive of highly varying day to day industrial activity and changing weather conditions. Elements such as S, Br and Pb were found higher in the PM2.5 (particulate matter with = 2.5 microm aerodynamic diameter), which are related to burning of coal and oil in furnaces in Mandi-Gobindgarh. The elements related to natural dust such as K, Ca, Ti, Mn, and Fe are mainly distributed in PMcf (particulate matter with aerodynamic diameter between 2.5 and 10 microm) fraction in both the towns. High concentrations of Ti, Cr, Mn, Fe and Zn in the PMcf fraction from Mandi-Gobindgarh are likely due to the industrial activity of Steel rolling mills.


Subject(s)
Aerosols , Air Pollutants/analysis , Arsenic/analysis , Bromine/analysis , Chlorine/analysis , Environmental Monitoring , India , Industry , Metals/analysis , Spectrometry, X-Ray Emission , Sulfur/analysis
4.
Article in English | IMSEAR | ID: sea-22851

ABSTRACT

BACKGROUND & OBJECTIVES: Irradiation with 131I is used for the treatment of various thyroid disorders. It is likely that radioiodine while in systemic circulation may cause some adverse effects on antioxidative enzymes present in red blood cells (RBCs). Zinc, on the other hand, has been reported to maintain the integrity of cells under certain toxic conditions. The present study was conducted to evaluate the adverse effects of 131I on RBCs and also to assess the protection provided by zinc under these conditions. METHODS: Female Wistar rats (n=32) were divided into four groups. Animals in group I served as normal controls; group II animals were administered a dose of 3.7 Mbq of 131I (carrier-free) intraperitoneally, group III animals were supplemented with zinc (227 mg/l drinking water) and animals in group IV were given a combined treatment of zinc as well as 131I. Activities of antioxidant enzymes were assessed in erythrocyte lysates after two days of treatments. RESULTS: An increase in the activity of glutathione reductase (GR), superoxide dismutase (SOD), reduced glutathione (GSH) and malondialdehyde (MDA) in the lysates of erythrocytes was seen after two days of exposure from 131I radiations. However, the activity of catalase was found to be significantly decreased. Interestingly, zinc supplementation to 131I treated rats resulted in attenuating the adverse effects caused by 131I on the levels of antioxidative enzymes. INTERPRETATION & CONCLUSION: 131I can induce significant oxidant/antioxidant changes in RBCs and zinc may prove to be a candidate with great promise for radioprotection.


Subject(s)
Animals , Catalase/blood , Erythrocytes/metabolism , Female , Iodine Radioisotopes/adverse effects , Malondialdehyde/analysis , Radiation-Protective Agents/pharmacology , Rats , Rats, Wistar , Superoxide Dismutase/blood , Zinc/pharmacology
5.
Indian J Exp Biol ; 2004 Oct; 42(10): 969-75
Article in English | IMSEAR | ID: sea-56714

ABSTRACT

This study was designed to determine the effect of nickel treatment on biological half-lives of 65Zn in whole body and liver as well as on distribution of 65Zn in different organs of protein deficient rats. Nickel sulfate at a dose level of 800mg/l in drinking water was administrated to normal control as well as to protein deficient rats for 8 weeks. A significant increase was found in fast and slow components of biological half lives of 65Zn in whole body and only fast component in liver of protein deficient rats. Interestingly, slow component in whole body and fast component in liver of nickel treated protein deficient rats were not different from normal controls though they were significantly elevated in protein deficient rats. On the other hand, slow component of 65Zn was also not altered in nickel treated protein deficient rats, which however, was significantly decreased in nickel treated rats. Protein deficiency led to a marked elevation in per cent uptake of 65Zn in brain and caused significant depression in liver, kidney and intestine. However, uptake of 65Zn in brain showed a significant depression in nickel treated rats, whereas the uptake was elevated in brain in nickel treated protein deficient rats. In conclusion, protein deficient conditions seem to be playing a dominant role in context with the distribution of 65Zn in different organs when nickel is administered to protein deficient rats. However nickel alone is seen to cause adverse effect on the distribution of 65Zn.


Subject(s)
Animals , Female , Half-Life , Liver/drug effects , Nickel/toxicity , Protein Deficiency/metabolism , Rats , Rats, Sprague-Dawley , Tissue Distribution , Zinc Radioisotopes/pharmacokinetics
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