Interaction of dietary calcium,manganese, and manganese source (Mn oxide or Mn methionine complex) on chick performance and manganese utilization

Two trials were conducted to determine the utilization of manganese (Mn) as influenced by the level and source of Mn and the level of dietary calcium (Ca) in broiler chickens. Trial One was a 2 x 2 x 3 factorial arrangement of two Mn sources (Mn methionine or manganous oxide), two levels of dietary Ca (1.8 or 1.0), and three levels of supplemental Mn (30, 60, or 200 mg/kg) fed until 4 wk of age. Total phosphorus (available phosphorus) levels were 0.70% (0.48%) during all ages. High levels of dietary Ca caused a slower early rate of growth (0.53 vs. 0.64 kg) for chicks fed 1.8 vs 1.0% Ca, respectively. Chick weight was equivalent for all diets within the Ca-treatment group, except the dietary combination of high Ca and 200 mg/kg Mn as Mn methionine. Bone and liver Mn were significantly increased as the Mn level increased, but were not affected by the Mn source. Chicks fed 1.8% Ca had higher levels of bone Mn (9.28 ppm) than chicks fed 1.0% Ca (7.23 ppm). High levels of dietary Ca and 200 ppm Mn methionine dramatically depressed early growth, feed intake, and bone ash in this trial, raising the question of a diet x environment (heat-stress) effect. Trial Two was a 2 x 2 factorial arrangement of two levels of dietary Ca (1.8 or 1.0%) and two Mn sources (200 mg/kg Mn as Mn methionine or MnO) up to 3 wk of age in a controlled heat-stress environment. No growth depression in the chicks fed high levels of Ca and Mn methionine was observed. In the presence of high levels of dietary Ca, bone Mn was significantly higher when chicks were fed the MnO source. In summary, dietary Ca did not decrease Mn utilization in these trials, and availability of Mn in Mn methionine as a source compared to MnO depended on dietary Ca levels.     

The fate of Cd,Cu, Ca,Zn, and Fe in rat during the recovery period following cessation of repeated exposure to Cd

Cadmium was administered subcutaneously to male Wistar rats, 0.1 mL/rat in 0.9% saline 3 times a wk for 4 wk at 3 mg Cd/kg. Saline was administered to control animals in an equivalent manner, without Cd. After the end of the dosing period, the distribution and excretion of Cd, Cu, Ca, Zn, and Fe were observed in some organs and excreta for 35 d (1, 7, 14, 21, 28, and 35 d). Cadmium dosing caused significant disturbances in the metabolism of Zn, Cu, Fe, and Ca, especially during the recovery period. Growth in Cd-dosed animals did not accelerate, even after 5 wk of recovery. There was evidence of mobilization of some elements among organs. Accumulation of Cd occurred in liver, kidney, and spleen during dosing, and during the recovery period it was retained in kidney and testes (for 2 wk) and cleared steadily in liver and RBC (for 5 wk), but increased in spleen (first 3 wk). The pattern of Cd excretion was closely associated with the binding of Cd with metallothioneins in kidney and liver for the first 21 and 7 d, respectively. This was associated with the excretion of Cd-metallothioneins (Cd-MT) in urine from d 1 to 21 during recovery. Cadmium caused higher Ca accumulations in testes and liver, which were probably associated with the lesions observed in these organs. Significant increases of Cu (in kidney d 7) and Fe (in liver) were observed during recovery. Furthermore, significant reductions of Cu and Fe were found in plasma, spleen, and RBC (after 5 wk) and kidney, spleen, and testes (on d 7), and blood (after 5 wk).     

Effects of Chronic Cadmium Poisoning on Zn, Cu, Fe, Ca, and Metallothionein in Liver and Kidney of Rats

An experiment was conducted to invest effects of chronic cadmium poisoning on Zn, Cu, Fe, Ca, and metallothionein gene expression and protein synthesis in liver and kidney in rats. Forty rats, 6?weeks old, were randomly allocated into two groups. A group was given CdCl(2) (1?mg/KgCd(2+)) by intraperitoneal injection once a day. The other group was treated with normal saline in the same way. Liver and kidney were collected for analysis at the end of the third week. Results showed that Cd exposure increased Cd (P?相似文献   

Distribution of 14 elements in various rat tissues following hypophysectomy,thyroparathyroidectomy, adrenalectomy,and castration

The tissue distribution of 14 elements was simulatneously determined in rats 28 d after hypophysectomy (HPY), thyroparathyroidectomy (TPTY), adrenalectomy (ADY), and castration (CTN). The elements Na, K, Ca, Mg, Fe, S, P, Rb, Sr, Mn, Cu, and Zn were investigated in whole blood, plasma, brain, liver, kidney, heart, skeletal muscle, and bone. Additionally Mo was determined in kidney and liver. The following results were obtained: 1) With regard to hormone deficiency: HPY induced the most noticeable, variations on all the elements tested owing probably to the direct and indirect effects of adenohypophyseal hormones. ADY led to the expected modification of Na and K but also to a Sr accumulation and a Rb depletion. TPTY induced a sharp decrease in plasma and tissues Ca, an increase in plasma P, but did not disturb the two elements in bone. An increase of Rb in many tissues and of Fe in heart, kidney, and liver were also observed. CTN had little consequences except in bone whose Cu and Fe contents were increased: 2) With regard to element variations: K, Mg, and S underwent little change. Discriminations were revealed between elements such as K and Rb, Ca and Sr, Ca and Mg, and Cu and Zn. The changes of Rb and Sr were consistent with regulatory mechanisms. The accumulation of Fe and Cu in tissues such as liver after HPY, TPTY, and ADY, suggest that the hormonal deficiencies could worsen the hemochromatosis with Wilson's disease; 3), With regard to plasma and tissues: No correlation appeared in element levels between plasma and other tissues. Brain was the least affected and liver, kidney and bone the most.     

Elemental alterations during the exposure of 1,2-dichloroethane (EDC), Disulfiram (DSF), and EDC-DSF to male Sprague-Dawley rats

Trace elements participate in the organ specific impact of 1,2-dichloroethane (EDC) and Disulfiram (tetraethylthiuram disulfide; Antabuse (DSF)) administered singly or together, on male Sprague-Dawley rats exposed by diet (AIN-76) to DSF (0 and 0.15% for 10 d before and during exposure to EDC) and by inhalation to EDC (0,153, 304, 455 ppm (v/v); 7 h/d for 5 d/wk for 30 exposure days). Kidney, liver, spleen, and testes at exposure d 30 as well as progressive urine samples were examined for elemental content by simultaneous inductively coupled plasma atomic emission spectroscopy. Each compound singly or together produced EDC dose related (r≥0.8) changes in metal content in organs relative to controls. There were increases induced by EDC alone for P and Sr in the liver and decreases for Fe, Mg, and P in the spleen. EDC in DSF-exposed animals caused increases in Ca, Cu, Fe, Mn, and S and a decrease in K in the liver; increases in Ca, Cu, Fe, Mn, Mo, P, and S and a decrease of Zn in the testes; an increase in Fe and a decrease in K in the spleen; and an increase of P in the kidney. DSF alone increased Cu in the liver but decreased it in the testes and kidney; Pb was increased in the liver and kidney and Zn in the liver, spleen, and kidney; Al and Si were increased also in the liver, S in the spleen, and K in the kidney; Mn and Na were decreased in the kidney. The organs showing histopathology (the liver and testes) both showed increases in Ca, Cu, Fe, Mn, and S. Metals in urine characterized a “shock” impact of the initial exposure by initial excretion of Na and retention of most other elements. After steady state (>12 d), EDC alone caused increases for Sr and Zn; for EDC-DSF, EDC also decreased Na in addition to the changes elicited by DSF alone (increases in S and Zn and a decrease for Cu). The results were interpreted from the perspective of the effects of metals on the glutathione detoxicative pathway, the concentration of free diethyldithiocarbamate in urine, and an interaction with bone. Mechanisms of action of EDC, DSF, and EDC-DSF must include consideration of trace elements in addition to organic intermediates, metabolites, and enzymes.     

Effects of Aluminum Exposure on Bone Mineral Density,Mineral, and Trace Elements in Rats

The purpose of the study was to investigate the effects of aluminum (Al) exposure on bone mineral elements, trace elements, and bone mineral density (BMD) in rats. One hundred Wistar rats were divided randomly into two groups. Experimental rats were given drinking water containing aluminum chloride (AlCl₃, 430 mg Al³⁺/L), whereas control rats were given distilled water for up to 150 days. Ten rats were sacrificed in each group every 30 days. The levels of Al, calcium (Ca), phosphorus (P), magnesium (Mg), zinc (Zn), iron (Fe), copper (Cu), manganese (Mn), selenium (Se), boron (B), and strontium (Sr) in bone and the BMD of femur were measured. Al-treated rats showed lower deposition of Ca, P, and Mg compared with control rats. Levels of trace elements (Zn, Fe, Cu, Mn, Se, B, and Sr) were significantly lower in the Al-treated group than in the control group from day 60, and the BMD of the femur metaphysis in the Al-treated group was significantly lower than in the control group on days 120 and 150. These findings indicate that long-term Al exposure reduces the levels of mineral and trace elements in bone. As a result, bone loss was induced (particularly in cancellous bone).     

Exendin-4, but not dipeptidyl peptidase IV inhibition, increases small intestinal mass in GK rats

Long-term treatment with dipeptidyl peptidase IV inhibitors (DPPIV-I) or glucagon-like peptide (GLP)-1 analogs may potentially affect intestinal growth by down- or upregulating the intestinotrophic hormone GLP-2. This study compared the intestinotrophic effects of 12-wk administration of vehicle, exendin-4 (Ex-4; 5 nmol/kg bid sc), or DPPIV-I (NN-7201, 10 mg/kg qd orally) in GK rats. Some animals were observed additionally for 9 wk after the end of treatment. Both treatments lowered glycated hemoglobin A1c at wk 12 vs. control (Ex-4, -0.8%; DPPIV-I, -0.4%). Body weight was reduced by Ex-4 compared with control (361 +/- 4 vs. 399 +/- 5 g; P < 0.001) because of reduced food intake, whereas neither parameter was affected by DPPIV-I. Linear bone growth was unaffected by either treatment. After treatment end, food intake in Ex-4 animals increased, and, by wk 21, body weight was identical in all groups. The small intestine of Ex-4-treated animals was larger at wk 12 compared with control (length, 135.6 +/- 1.6 vs. 124.5 +/- 2.3 cm, P < 0.001; absolute weight, 8.4 +/- 0.2 vs. 6.4 +/- 0.4 g, P < 0.001), being most pronounced proximally, where the absolute cross-sectional area related to body weight increased by 24% because of increased mucosal thickness. These effects were reversible, and 9 wk after the end of treatment, no differences between Ex-4 and control were apparent. Plasma GLP-2 concentrations were unaltered by either treatment, and Ex-4 had no agonistic or antagonistic effects on the transfected GLP-2 receptor. DPPIV-I had no intestinal effects. In conclusion, the continued presence of Ex-4 is necessary to maintain weight loss in GK rats. Effective antihyperglycemic treatment with Ex-4 increases intestinal mass reversibly, whereas DPPIV-I lacks intestinal effects.     

Effect of cadmium and aluminum intake on the antioxidant status and lipid peroxidation in rat tissues.

This work aimed to study the relationship between the accumulation of cadmium (Cd) or aluminum (Al) in certain tissues and the levels of lipid peroxides as well as tissue antioxidants. To carry out such investigations, CdCl2 was given to rats in two dose levels; 0.5 or 2.0 mg/kg i.p for 1 day or daily repeated doses for 2 weeks. Al was given as AlCl3 either in a single dose of 100 mg/kg or daily repeated doses of 20 mg/kg for 2 and 4 weeks. The measured parameters were tissue malondialdehyde (MDA, index of lipid peroxidation) and reduced glutathione (GSH) levels as well as the activities of glutathione peroxidase (GSH-PX), glutathione reductase (GSSG-R), and glucose-6-phosphate dehydrogenase (G-6-PDH) enzymes. Liver and kidney functions were assessed by measuring serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities as well as serum urea and creatinine concentrations. Cd and Al concentrations in the studied tissues were also measured. Results indicated that tissue Cd was significantly increased after administration of either Cd doses. After a single dose of 0.5 or 2.0 mg/kg CdCl2, the increase in tissue Cd levels were accompanied by an increase in MDA and a decrease in GSH levels. On the other hand, after repeated administration of Cd, tissue Cd accumulation was accompanied by increased hepatic and renal GSH levels with decrease in MDA content and a decrease in GSH-PX activity in liver. Liver function was affected at all dose regimens, whereas kidney function was affected only after 2 weeks administration of the higher dose. In Al treated rats, Al concentration was shown to be increased in liver much more than in brain. This was accompanied by a slight decrease in hepatic GSH level after 2 weeks and a decrease in GSH-PX activity after 4 weeks. Liver function was affected only after repeated injection of Al for 2 or 4 weeks. In general, Al administration exhibited safer pattern than Cd.     

Feeding of a low-zinc diet lowers the tissue concentrations of alpha-tocopherol in adult rats

Previous work has shown that a low dietary intake of zinc for a short duration significantly lowers the lymphatic absorption of α-tocopherol (αTP) in adult male rats. The present study investigated whether the nutritional status of zinc is critical in maintaining the tissue levels of the vitamin. One group of rats was fed an AIN-93G diet containing 3 mg zinc/kg (low zinc, LZ) and the other was fed the same diet but containing 30 mg zinc/kg (adequate zinc, AZ). Food intakes between groups were matched by feeding two meals per day. At 6 wk, the body weights (356±8 g) of LZ rats reached 98% those (362±10 g) of AZ rats. Feeding of the LZ diet for 6 wk significantly lowered the concentrations of both αTP and zinc in the liver, kidney, heart, testis, and brain. No consistent relationships between αTP and zinc concentrations were observed in other tissues such as spleen, lung, gastrocnemius muscle, and retroperitoneal fat tissues. The concentrations of αTP in the liver, testis, brain, spleen, heart, and kidney were significantly correlated with the tissue concentrations of zinc. The LZ diet slightly but significantly increased the total lipid contents (mg/g) of liver, kidney, heart, and spleen. However, the tissue levels of phospholipid (μmol/100 mg lipid) in the heart, lung, testis, and spleen were decreased significantly in LZ rats. These findings indicate that low zinc intake results in a pronounced decrease in the animal’s αTP status under the conditions of matched food intakes, body weights, and feeding patterns. The lower tissue levels of αTP may explain in part the compromised antioxidant defense system and increased susceptibility to oxidative damage observed in zinc deficiency.     

Excess calcium increases bone zinc concentration without affecting zinc absorption in rats

We examined zinc (Zn) metabolism in rats given diets containing excess calcium (Ca). Rats were given phytate-free diet containing 5 g Ca/kg (control), 12.5 g Ca/kg, or 25 g Ca/kg for 4 wk in Experiment 1. The dietary treatment did not affect Zn concentration in the plasma, testis, kidney, spleen and liver; however, Zn concentration in the femur and its cortex was significantly higher in rats given diet containing 25 g Ca/kg than in other rats. Rats were given phytate-free diet containing 5 g Ca /kg or 25 g Ca /kg for 4 wk in Experiment 2. After 12-h food deprivation, rats were given a diet extrinsically labeled by 67Zn with dysprosium as a fecal marker for 4 h. Feces were collected from 1 d before administration of the labeled diet to 5 d after administration. Excess Ca did not affect the true absorption of Zn and its endogenous excretion but increased femoral Zn. These results suggest that excess Ca improves Zn bioavailability without affecting Zn absorption when diets do not contain phytate.     

Chronic effects of cadmium on kidney,liver, testis,and fertility of male rats

Male Wistar rats (n:20), at 5 wk of age, were given cadmium in drinking water (10 mg/L water) for 52 wk; 8 males and 20 female rats, as controls, were given tap water. At the end of 28 and 40 wk, some of the cadmium-treated males and control group male rats were sacrificed for the histopathological examination of testis, kidney, and liver. At the end of 56 wk, histopathological examinations were performed in the same way. Liver, kidney, and testis cadmium levels were also determined by atomic absorption spectrophotometry. All the cadmium-treated male rats showed pathological testicular alterations, and liver and kidney damage after chronic exposure. Cadmium levels were found to be highest in the kidney (1.009 +/- 0.034 microgram/g wet tissue in the infertile group). At the end of the 52-wk period, reproductive capacity of the cadmium-treated rats was investigated and was found to be lost in 39.89% of the animals.     

Proliferation patterns of latent Pneumocystis carinii in rat organs during progressive stages of immunosuppression

Pneumocystis carinii is known to proliferate mainly in the lung of an immunocompromised host. In AIDS and other immune disorders sporadic extrapulmonary presence of this organism has been documented. Occasionally, P. carinii does not appear to infect the lung. These observations have been based on the detection of P. carinii by conventional staining techniques. We have sought to determine the extent of these infections by the polymerase chain reaction (PCR) in a rat model. Harlan Sprague-Dawley rats weighing between 110 and 130 g were immunosuppressed with dexamethasone (1.2 mg/l) in drinking water. During progressive stages of immunosuppression 2 rats were sacrificed at 2, 3, 4 and 5 wk, and the lung, liver, kidney, spleen and bone marrow were taken. Sonicated crude extracts of the tissues were used as template DNA for the amplification of the dihydrofolate reductase (DHFR) gene of P. carinii. All the PCR products were analyzed by Southern hybridization with radiolabelled DHFR DNA. These analyses revealed a general trend of P. carinii proliferation first in bone marrow at 2 wk, followed by liver at 3 wk, and lung at 5 wk on immunosuppression. Kidney and spleen infections were infrequent. Although P. carinii appears to proliferate in the lung at later stages of immunosuppression, the degree of proliferation is several-fold greater than in extrapulmonary organs. The extrapulmonary proliferation of P. carinii, however small, may possibly suppress hematopoietic stem cell differentiation in bone marrow, and may also contribute to the pathology present in various organs.     

Aluminium accumulates on inactive bone surfaces after parathyroidectomy in uremic rats

In recent studies on bone biopsies of long-term hemodialyzed patients, parathyroidectomy (PTx) has been shown to represent a risk factor for subsequent accumulation of aluminium (Al) in the bone. Therefore, the influence of late PTx on Al metabolism in uremic rats previously given 11 mg Al intraperitoneally during a period of four weeks was studied. Al content was determined in the blood, liver, bone and feces 7 and 14 days after PTx. During PTx, each animal also received 2 intramuscular implants of partially demineralized bone matrix cylinders, which served as inactive bone surfaces. In PTx animals, the Al content in the liver, spleen and kidney progressively decreased, while its blood levels increased in spite of the fact that the treatment was stopped. Bone values remained unchanged but Al markedly accumulated on inactive mineralized surfaces of implanted cylinders. Significant amounts of Al in fecal masses could indicate its biliary excretion. The results were influenced neither by changes in 1,25-(OH)2D3 or serum calcium values, nor by different degrees of renal failure after PTx. It is suggested that accumulation of Al in the bone after PTx, as found in dialyzed patients, constitutes a passive event triggered by inactive bone tissue.     

The Effects of Glutamate and Citrate on Absorption and Distribution of Aluminum in Rats

The objective of this study was to evaluate the effect of glutamate (Glu) and citrate (Cit) on the absorption and distribution of aluminum in rats. In the in vitro experiment, 18 adult male Sprague-Dawley rats (average weight of 250 ± 15 g) were randomly divided into three groups. The entire intestine was rapidly removed and cultured in prediction samples of 20 mmol AlCl(3), 20 mmol AlCl(3)+20 mmol Cit, and 20 mmol AlCl(3)+20 mmol Glu, respectively. Liquid in different intestines and the intestines were obtained for Al determination. In the in vivo chronic study, 24 adult male Sprague-Dawley rats (average weight of 127 ± 10 g) were divided into four groups fed with the following diets: no Al and Glu added (control), AlCl(3) (1.2 mmol), AlCl(3) (1.2 mmol) + Cit (1.2 mmol), and AlCl(3) (1.2 mmol) + Glu (1.2 mmol) daily for 50 days, respectively. After rat sacrifice, blood samples were obtained for biochemical analyses, and organ samples like the brain, kidney, liver, and bone were rapidly taken for Al determination. The results showed that the absorption rate of Al with the following order: duodenum > jejunum > ileum in the in vitro study and the administration of AlCl(3)+Cit or AlCl(3)+Glu resulted in significant increases in Al absorption in the three parts of the gut (duodenum, jejunum, and ileum) compared to the AlCl(3) alone group based on wet weight (P < 0.05). There were no differences between the AlCl(3)+Cit and AlCl(3)+Glu groups. In the in vivo chronic study, supplementing either AlCl(3) alone or AlCl(3)+Glu decreased food consumption significantly (P < 0.05) compared with the control group. Compared with the control group, animals fed with the AlCl(3) diet monitored for red blood cell, kidney, and liver showed a higher level (P < 0.05), but did not significantly increase Al retention in the brain and bone (P > 0.05); animals fed with AlCl(3)+Cit diets were monitored for higher Al retention in the brain, kidney, bone, and liver (P < 0.05), while animals fed with AlCl(3)+Glu diets were monitored for red blood cell, brain, and kidney (P < 0.05). Compared with the AlCl(3) group, simultaneous administration of AlCl(3) and Glu led to a significant increase in Al retention in red blood cell, brain, and kidney (P < 0.01) while AlCl(3) and Cit in the kidney and bone (P < 0.01). Simultaneous administration of AlCl(3) and Cit significantly increases plasma malondialdehyde level (P < 0.05); both simultaneous administration of AlCl(3) and Glu or AlCl(3) and Cit led to significant decreases in superoxide dismutase level in the plasma (P < 0.05), while AlCl3 alone did not. The results indicated that both Cit and Glu enhanced Al absorption in the intestine in vitro, and Glu increased Al deposition in red blood cell, brain, and kidney in vivo.     

Osteoporotic cytokines and bone metabolism on rats with induced hyperthyroidism; changes as a result of reversal to euthyroidism

Hyperthyroidism is characterized by increased bone turnover and resorptive activity. Raised levels of serum osteoporotic cytokines, such as interleukin (IL) -1beta, IL-6 and tumor necrosis factor (TNF)-alpha have been demonstrated previously in hyperthyroidism. These elevations are controversial and it is difficult to differentiate the contribution of thyroid hormones to the elevation of cytokines from that of the autoimmune inflammation in Graves' disease (GD) and follicular cell damage in thyroiditis. Therefore, we investigated the effect of thyroid hormones on serum IL-1beta, IL-6, TNF-alpha levels and bone metabolism on L-thyroxine induced hyperthyroid rats and changes in cytokine levels and bone metabolism on the same rats after reversal to euthyroidism. Rats were treated with L-thyroxine for 5 weeks (0.4 mg/ 100 g food). Plasma T3, T4, TSH and serum IL-1beta, IL-6, TNFalpha, Calcium (Ca), phosphorous (P), parathyroid hormone (PTH), alkaline phosphatase (ALP), bone alkaline phosphatase (B-ALP) levels were measured and differential leucocyte counts were made initially, at the 5th week of the experiment (hyperthyroid state) and 5 weeks after quitting the administration of L-thyroxine (euthyroid state). Significant rises in serum IL-1beta, IL-6 and TNFalpha were noted in hyperthyroidism (P < 0.001). In euthyroid state, IL-15, IL-6 and TNFalpha decreased significantly, but IL-beta and TNFalpha were significantly higher than the baseline values (P < 0.05) while IL-6 levels turned back to the baseline values. Plasma T3 and T4 levels were significantly correlated with serum cytokines in hyperthyroid state while there was no correlation in euthyroid states. Ca and P levels did not differ significantly while PTH levels declined significantly in the hyperthyroid state (P < 0.05). After the reversal to the euthyroidism, there was no significant change in Ca, P and PTH levels. ALP and B-ALP increased significantly in hyperthyroidism (P < 0.001, P < 0.01) and they did not decrease in euthyroid state. The lymphocyte number and ratio in differentials increased significantly in the hyperthyroid state (P < 0.001). In euthyroidism they decreased significantly (P < 0.001) but it was significantly higher than the baseline value (P < 0.05). Our findings showed that the deleterious effect on bone metabolism in hyperthyroidism might be mediated by cytokines and the increased bone turnover in hyperthyroidism failed to decrease despite euthyroidism.     

Effects of oral aluminum on essential trace elements metabolism during pregnancy

The present study was conducted to assess in rats the effects of oral aluminum (Al) exposure on calcium (Ca), magnesium (Mg), manganese (Mn), copper (Cu), zinc (Zn), and iron (Fe) accumulation and urinary excretion. Three groups of plug-positive Sprague-Dawley (SD) rats were given by gavage 0, 200, and 400 mg/kg/d of Al(OH)₃ on gestational days 1–20. Three groups of nonpregnant female SD rats of the same age received Al(OH)₃ by gavage at the same doses for 20 consecutive days. At the end of the treatment period, 24-h urine samples were collected for analysis of Al and essential elements. Subsequently, all animals were sacrificed and samples of liver, bone, spleen, kidneys, and brain were removed for metal analyses. With some exceptions, the urinary amounts of Al, Mn, and Cu excreted by pregnant animals as well as the urinary levels of Al excreted by nonpregnant rats were higher in the Al-treated groups than in the respective control groups. Although higher Al levels were found in the liver of pregnant rats, the concentrations of Al in the brain of these animals were lower than those found in the same tissues of nonpregnant rats. With regard to the essential elements, tissue accumulation was most affected in pregnant than in nonpregnant animals. In pregnant rats, the hepatic and renal concentrations of Ca, Mg, Mn, Cu, Zn, and Fe, as well as the levels of Ca in bone, and the concentrations of Cu in brain were significantly higher in the Al-exposed groups than in the control group. According to the current results, oral Al exposure during pregnancy can produce significant changes in the tissue distribution of a number of essential elements.     

Stimulatory effect of calcium administration on regucalcin mRNA expression is attenuated in the kidney cortex of rats ingested with saline

The expression of calcium-binding protein regucalcin mRNA in the kidney cortex of rats ingested with saline was investigated. The alteration in regucalcin mRNA levels was analyzed by Northern blotting using liver regucalcin complementary DNA (0.9 kb of open reading frame). Rats were freely given saline as drinking water for 7 days. Regucalcin mRNA levels in the kidney cortex were suppressed by saline ingestion. When calcium chloride (10 mg Ca/100 g body weight) was intraperitoneally administered to rats ingested with saline for 7 days, the effect of calcium administration to increase regucalcin mRNA levels was weakened by saline ingestion. Such effect was also seen by the administration of 2.5 and 5 mg Ca/100 g. Regucalcin mRNA levels in the kidney cortex of spontaneous hypertensive rats (SHR) were not appreciably increased by the administration of calcium (10 mg/100 g). Meanwhile, calcium content in the kidney cortex was significantly elevated by the administration of calcium (10 mg/100 g) to normal rats. This increase was weakened in saline-ingested rats. Moreover, Ca²⁺/calmodulin-dependent protein kinase activity in the cytosol of kidney cortex was significantly decreased by saline ingestion. These results suggest the possibility that saline ingestion-induced suppression of regucalcin mRNA expression in the kidney cortex is partly involved in the attenuation of Ca²⁺ signalling.     

New experimental observation on the relationship of selenium and diabetes mellitus

Selenium shows insulin-mimic properties in vitro and in vivo. However, in this study, a high dose of 4 mg/kg/d selenite orally administered to the alloxan-induced diabetic Kun-Ming mice for 4 wk failed to reduce hyperglycemia. Se contents in plasma and tissues such as the liver, kidney, spleen, and brain were determined and the thiobarbituric acid-reactive substances (TBARS) levels were investigated. The results showed that alloxan-induced diabetes did not cause a significant decrease in Se levels in plasma and the above tissues compared to the normal control, but selenite treatment significantly increased Se levels in plasma, liver, and brain of the selenite-treated diabetic mice compared to the nontreated diabetic mice. In addition, selenite treatment for diabetic mice reduced the TBARS levels in red blood cells (RBCs) compared to the normal and improved the glutathione peroxidase (GSH-Px) levels in RBCs significantly compared to the diabetic control. In conclusion, this study demonstrated that although oral administration of a high dose of selenite had no hypoglycemic effect on diabetic mice in 4 wk, selenite treatment still maintained the antioxidant beneficial effect on the diabetic mice. This study shed more light on the relationship between Se and diabetes.     

Effects of dietary chromium chloride supplementation on performance,some serum parameters,and immune response in broilers

This study was conducted to investigate the effect of increasing dietary levels of inorganic chromium (CrCl₃·6H₂O) on the performance, blood chemistry, and immune response of broilers. Eighty newly hatched Ross PM3 broiler chicks were evenly distributed to five groups of 16 chicks each. Two groups (control and only sheep red blood cell inoculated) were fed the basal diet containing 2.2 and 4.5 mg Cr/kg and the remaining groups were fed 20, 40, or 80 mg/kg Cr-supplemented diets for 44 d. Chicks in all groups, except in the control, at 3 and 5 wk of age, were injected intraperitonally with sheep red blood cell for determining the primary and secondary antibody responses, respectively. When the chicks were 4 wk of age, a delayed-type hypersensitivity test was performed. White blood cells were differentiated. Blood samples were collected for the determination of serum proteins, glucose, cholesterol, cortisol, minerals, and alkaline phosphatase activity and for antibody response. Chromium had no effect on weight gain, but 20 mg/kg supplemental Cr resulted in 18.57% reduction in feed consumption and improved feed efficiency by 16.77%. Chromium did not affect serum cholesterol and P levels but reduced serum glucose and increased serum protein, Cr, Ca, and Mg levels, and ALP activity. A slight reduction was observed with Cr supplementation in cortisol levels. Slight but not significant increases were observed with Cr in serum Zn and Cu. Chromium increased the ratio of bursa of Fabricius and liver to body weight. Heterophil and monocyte counts and heterophil/lymphocyte ratio were reduced and lymphocyte counts, total antibody, IgG, and IgM titers were increased by supplemental Cr. All levels of Cr increased the cell-mediated response to phytohemagglutinin. No alterations in tissues were observed by histopathological examinations.