study of indium distributions in rat liver, kidney and brain tissues

Indium belonging to group IIIa, which is used in different industries and medical science. Therefore toxicity with this element is predictable. In this study, we to measure the concentration of indium in kidney, liver and brain. Pathological effects of indium to these tissues also have been studied. After determination of LD50, 0.35-mg/Kg indium as InC13 was injected [I.P] daily to rats for 60 days. Concentration of indium in serum and hemogenate of liver, kidney and brain tissues determined by flameless atomic absorption, showed that indium concentration is more in the kidney and liver. Also, microscopic examination of these tissues shows increase damage of these two organs. From forgoing results, we came to conclusion that damages caused by indium on these tissues is probably depend to the indium concentration in its

Study of the effect of residual chlorine on serum iron and related parameters

The major purpose of the present investigation was to study the effects of different concentrations of residual chlorine on serum iron related parameters in rats. Feeding male rats with water containing 80 ppm of residual chlorine daily for 5 days reduced serum levels of ceruloplasmin, copper, iron and hemoglobin by approximately 27%, 23%, 6% and 4%, respectively. Higher reductions in serum ceruloplasmin [35%], copper [50%], Fe [17%] and hemoglobin [14%] were observed when rats were given water containing 160 ppm of residual chlorine daily for 5 days. The total iron binding capacity [TIBC] level was elevated by 9 and/or 13% respectively. Daily feeding of rats for 10 days with water containing 160 ppm residual chlorine caused significant reductions in serum levels of ceruloplas min [50%], copper [54%] iron [17%] and hemoglobin [17%]. Serum TIBC was elevated by 25%. Long term effects of residual chlorine on the above parameters were also investigated. It can therefore be concluded that residual chlorine in drinking water may interfere with iron metabolism. The relationship between the occurrence of anemia and residual chlorine toxicity has been discussed

Development of a method for aluminum determination in serum and dialysis by flameless atomic absorption with graphite furnace

Aluminium determination was carried out in serum and dialysis fluid by a simple and reliable method of flameless atomic absorption with graphite furnace. No preparatory procedures are required for water and dialysis fluid. In this method serum was mixed with 0.2% HNO3 to allow complete combustion of the samples in order to improve analytical precision. The method has a sensitivity of 15 pg and detection limit of 2.1 micro g Al/L. The aluminium contents of the main water supply, be-distilled water and dialysis fluid were 52, 1, and 44 micro g/L respectively. The mean value for normal serum aluminium in Isfahan was 3.6 micro g/L. Serum aluminium concentration in chronic renal failure was measured in pre- and post-dialysis samples. The mean values for the serum aluminium levels pre- and post-dialysis were 30.5 and 71.08 micro g/L with a range of 9-60 and 21-123 micro g/L, respectively. Pre- and post-dialysis serum aluminium values in female patients were within the range of 1-42 and 12 66 micro g/L with mean values of 18.25 and 40.5 micro g/L, respectively. Instrumental settings and sample handling are discussed

Aluminum toxicity: a review in relation to chronic renal failure patients maintained on regular hemodialysis

Aluminum is present in very small amounts in living organisms but abundant in the environment. A growing literature links with the biochemistry of aluminum and also with a series of diseases in chronic renal failure patients on treatment with hemodialysis. The initial description of potential aluminum toxicity in renal failure patients relates to description of dialysis encephalopathy syndrome in 1972. the major emphasise of this review will be on the recent literature involving aluminum metabolism and epidemiology of aluminum related disease. Finally the possibility that aluminum contributes to hypochromic microcytic anemia, dialysis osteomalacia [Newcastle bone disease], encephalopathy and Alzheimer disease in hemodialyzed patients has been also discussed

How aluminum is taken up by red blood cells: a study in relation to hypochromic microcytic anemia in hemodialyzed patients

Investigation of aluminium uptake by human erythrocytes was the major aim of this study. Packed red blood cells were incubated in Earle's medium [pH 7.4] containing varying concentrations of aluminium [0-160 micro g/l] as A1K[SO[4]][2] and aluminium content of the cells were determined using flameless atomic absorption. There was significant increase in aluminium content of the cells. Addition of 5 mM glucose caused an elevation of red cell aluminium, whereas depletion of red cells from ATP caused a marked reduction in aluminium uptake. Both ouabain and vanadate, when added to the medium, caused a significant reduction in aluminium uptake in line with a decrease in ATP ase activity

effect of aluminum on biochemical parameters related to bone metabolism: a model study of hemodialysis patients

The influence of aluminum on some serum parameters related to bone metabolism has been investigated by daily administration of aluminum over different periods of time. Daily administration of aluminum [1 mg/kg BW] for 20 or 50 days elevated serum phosphorous concentration by 16 percent and had no significant effect on serum calcium level. When aluminum was injected as a complex with citric acid [1:1] there was a 22 percent elevation in serum phosphorous concentration, but again had no significant effect on serum calcium. Same amounts of aluminum caused a 28 percent elevation in serum alkaline phosphatase [ALKP], but had no significant effect on serum parathormone [PTH] either with or without citric acid. A marked reduction [about 41 percent] in serum calcitonin was observed when rats were given aluminum with or without citric acid. The relationship between aluminum toxicity and osteomalacia has been discussed