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

[ effect of titanium on stearic acid transport in rat everted gut sac]

Background and Objective: an everted intestinal sac [EGS] technique has been used to extensively estimate the transport and intestinal absorption in rats. Therefore, a number of factors such as pH and the nature of solvent may play an important role in fatty acid uptake by enterocytes. There are reports indicating that fatty acid transport is affected by many biochemical parameters including trace elements. In this study the effect of titanium on stearic acid transport was investigated

Materials and Methods: wistar male rats [200-250gr] were used for the experiments. Rats were killed, their intestine was removed and the jejunum parts were dissected. Everted gut sac was prepared from these parts. Sacs full of buffer were incubated in a medium containing stearic acid and titanium. Then the transported stearic acid inside the EGS was measured by spectrophotometer under different conditions of temperature and concentrations. Data was analyzed using SPSS software and Mann Whitney test

Results: the results showed that titanium decreased fatty acid uptake by enterocytes in a dose dependent manner. Titanium concentrations of 0.5, 1, 1.5 and 10 micromoles in the presence of sodium chloride can decrease the uptake of stearic acid by 32.2%, 43.4%, 54.5% and 61.5%, respectively. Titanium concentrations of 0.5, 1, 1.5 and 10 micromoles in the absence of sodium chloride in medium could decrease the stearic acid by 10%, 19.5%, 23.9% and 28.3% respectively which is not very affective

Conclusion: stearic acid transport appeared to be a Na dependent process and titanium may exert its inhibitory effect by interfering with this system. Our results showed that the incubation time, stearic acid concentration and pH were effective on stearic acid transport. Titanium decreased stearic acid transport in Rat EGS. This should be considered seriously, especially in people exposed to titanium compounds for a long period

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

Comprehensive study of some plasma biochemical parameters in relation to bone disease in hemodialysis patients in Isfahan

The concentrations of serum calcitonin, parathormone [PTH], amylase, alkaline phosphatase [ALKP], calcium and phosphorus were studied in pre-and post-dialysis patients with chronic renal failure. All patients had extremely elevated serum urea and creatinine concentrations with the mean values of 143.8 and 10.5 mg/dL respectively. The plasma amylase activity was higher than normal with a mean of 174 lU/L, but showed no significant changes following hemodialysis. The mean values for calcium and phosphorus in predialysis plasma were 7.2 and 7.5 mg/dL respectively, whereas it changed to 8.6 and 3.8 mg/dL post-dialysis. The extent of increase in PTH and alkaline phosphatase levels depended on the duration of dialysis in the majority of the patients. The longer the period of the dialysis, the higher the concentrations of PTH and ALKP. On the basis of this study the relationship between bone disease and hemodialysis has been discussed

Study of the relationship between aluminium toxicity and heme synthesis

In relation to chronic hemodialysis patients with aluminum overload, the effects of free and protein bound fractions of aluminum on iron uptake, heme synthesis and ferrochelatase activity were studied. The iron uptake by mitochondria was found to be a time dependent process and depended on the degree of saturation of transferring with iron. Aluminum, as a complex with transferrin, significantly reduced iron uptake and heme synthesis by mitochondria. Aluminum did not alter the ferrochelatase activity. Thus the possibility that the disturbances of heme synthesis in hemodialysis patients may be due to aluminum toxicity is discussed

Chromium interaction with iron metabolism in rat: a model study in relation to hemodialysis patients

The interaction between chromium and some serum iron related parameters were investigated. Intraperitoneal administration of 1 mg/kg chromium [as chromium chloride] for 45 days reduced the serum iron and total iron binding capacity by 27% and 11% respectively. Ferritin and hemoglobin concentrations were also reduced by 22% and 18%, respectively. The results suggest that chromium influences iron metabolism and these two elements are biochemically interrelated