Our work represents a comprehensive and interdisciplinary effort toward better understanding, which attributes of guidelines have the potential to improve uptake in clinical practice. We also created codebooks and narratives of key concepts, which can be used to create tools for developing better guidelines to promote better care.

Arsenic is a potent toxin, carcinogen and modulator of antioxidant defense system. In this study, male rats of Wistar strain, maintained on either 18% or 6% protein (casein) diet, received an acute i.p. exposure to sodium arsenite (As3+) at its LD50 dose (15.86 mg/kg body weight). One hour after the arsenic exposure, glutathione (GSH) concentration was significantly depleted and lipid peroxidation was increased. A relationship between any two of tissue arsenic concentrations, GSH levels and lipid peroxidation values was observed only for liver when the proportional changes of respective parameters in either of the dietary groups of animals were compared. This suggests that, in liver, arsenic metabolism appears dependant upon the GSH concentration. Acute arsenic exposure significantly increased the glutathione peroxidase (GPx) activity in liver of both dietary groups and in kidney of only the 18% protein-fed group of animals. The glutathione-S-transferase (GST) activity significantly decreased in liver of the 18% protein-fed animals while GST increased in kidney of both the 18% and the 6% protein-fed groups. No significant change in glutathione reductase (GR) or glucose-6-phosphate dehydrogenase (G6PDH) activity was observed. In the present investigation, liver as a whole seems to be more affected in terms of GSH level and GST activity. The mode of responses of GPx and GR activities as well as the unaltered G6PDH activity might result in arsenic-induced GSH depletion and increase in lipid peroxidation. The animals of the 6% protein-fed group, appeared to be affected less in terms of tissue arsenic concentration, GSH level and GST activity. lipid peroxidation,

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This study was initiated to examine the extent of toxic metal contamination of the east Calcutta wetland ecosystem. Biological oxygen demand, chemical oxygen demand, total dissolved solids, conductivity, total suspended solids, total hardness, and pH were recorded from six different locations on the sewage carrying canals including an industrial effluent-fed fish pond in the eastern Calcutta (lat. 22°33´-22°40´ N; long. 88°25´-88°35´ E). Concentrations of metals such as Pb, Cu, Cr, Zn, Fe, Mg, and Mn in wastewater, and water of adjacent sewage-fed fish tank were also determined. Concentrations of these metals in soil/sludge and accumulation of these metals in plant and fish tissues were also studied. The concentrations of heavy metals in wastewater, namely Pb, Zn, Cu, Mn, and Fe, were reduced by 25 to 45% and total Cr was reduced by 95%, on the course of the 40 km long journey of the composite wastewater from the sources to river mouth via the wastewater carrying canal and the stabilization pond. Reductions of 65% Zn and 99% Cr in soil/sediment were recorded between sources and final discharge sites.

The effects of melatonin on arsenic-induced changes on cellular antioxidant system were studied in male rats of the Wistar strain. Arsenic treatment (i.p. as sodium arsenite) was done at a dose of 5.55 mg/kg body weight (equivalent to 35% of LD50) per day for a period of 30 days, while melatonin supplementation (i.p.) was performed at a dose of 10 mg/kg body weight per day for the last 5 days prior to sacrifice. Melatonin supplementation reversed the arsenic-mediated changes in reduced glutathione (GSH) level and lipid peroxidation in liver and kidney. Arsenic-induced decreased glutathione reductase activity in liver and increased activity in kidney was appreciably counteracted by melatonin. Melatonin also inhibited arsenic-induced free hydroxyl radical production in the tissues. The decreased superoxide dismutase (SOD) activity in liver and kidney and that of catalase in liver due to arsenic treatment were also counteracted by melatonin. It is suggested that melatonin acts as a protective agent against arsenic-induced cellular oxidative stress.

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