Influence of cadmium and zinc on the mice resistance to Listeria monocytogenes infection.
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The objective of this study was to examine the effect of chronic exposure to cadmium and zinc on the mice resistance to experimental Listeria monocytogenes infection. MATERIALS AND METHODS: At the day beginning of experiment outbred mice were injected with suspension of bacteria and 8 weeks were given the following oral intake treatment: control group (n=28) deionized drinking water, Cd- group (n=37) water containing CdCl2 10 mg/l and Cd+Zn- group (n=33) water containing CdCl2 10 mg/l and ZnSO4 100 mg/l. The delayed type hypersensitivity was evaluated by the inflammatory response during so-called "foot" test. Listerial proteins solution was injected under plantare of lower aponeurosis of rear foot of experimental animals. Survival of L. monocytogenes in organs of experimental animals was evaluated by the presence of bacteria colonies after 30 days incubation of livers homogenates in broth medium at +4 degrees C and inoculation on CASO-agar. Kidneys, liver and spleen were used for metals analysis. Differences were significant if the P value was below 0.05. RESULTS: Chronic exposure to Cd or to Cd with Zn for 8 weeks caused influence on survival of mice: Cd- and Cd+Zn groups mice died more rapidly than control group ones. Bacterial growth in organs was observed for all groups until fourth week. From sixth-week, control and Cd+Zn- group's mice more rapidly eliminated bacteria from organs, demonstrating that Zn- treated mice were more resistant to listerial infection than Cd- intoxicated ones. On the other hand, mice from Cd+Zn- group had significantly decreased spleen index (up to 74%, p<0.01) as compared to control group. Chronic poisoning of mice with low doses cadmium and zinc during infection significantly affected (p<0.05) their growth rate from fourth week in both experimental groups. Cadmium and zinc insignificantly decreased the delayed type hypersensitivity response to L. monocytogenes allergens in Cd+Zn- group of mice, and no differences were observed in Cd- group, as compared with control group. CONCLUSIONS: 1. Cadmium-exposed mice are more susceptible to Listeria monocytogenes and to other opportunistic infections than not intoxicated mice. 2. Zinc significantly reduces the negative effect of cadmium on the antimicrobial defense of mice. 3. Cadmium and zinc no significantly decrease the delayed type hypersensitivity response to L. monocytogenes allergens as compared with control. (+info)
Follow up study of renal tubular dysfunction and mortality in residents of an area polluted with cadmium.
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A retrospective cohort study was conducted to investigate the association between cadmium induced renal tubular dysfunction and mortality. A total of 230 subjects aged 40 or older and living in a cadmium polluted area in Kosaka Town, Akita Prefecture, Japan, were studied at least once between 1975 and 1977 and again in 1990. Urinary beta 2-microglobulin and total amino nitrogen concentrations were significantly related to mortality from all causes in women. The finding supports the idea that cadmium induced kidney damage is a factor associated with mortality in a general population exposed to environmental cadmium. (+info)
Protective effects of fulvotomentosides on cadmium-induced hepatotoxicity.
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Fulvotomentosides (Ful) is the total saponins of Lonicera fulvotomentosa. In the present study, we examined the effects of Ful on cadmium (CdCl2)-induced acute liver injury in mice. Ful pretreatment (150 mg.kg-1, sc x 3 d) remarkably decreased CdCl2 (3.7 mg Cd.kg-1, iv)-induced liver damage as indicated by serum activities of alanine aminotransferase and sorbitol dehydrogenase. Distribution of Cd to 12 organs and hepatic subcellular fractions was determined 2 h after Cd challenge. Ful pretreatment did not produce a marked shift in the distribution of Cd to various organs, but markedly altered the hepatic subcellular distribution of Cd, with more Cd bound to metallothionein (MT) in the cytosol, less in the nuclear, mitochondrial, and microsomal fractions. Ful pretreatment produced a dose-dependent increase in hepatic MT as determined by the Cd.hemoglobin assay. In conclusion, Ful protected against Cd hepatotoxicity by inducing MT, which binds Cd in the cytosol and lowers the amount of Cd available to other critical organelles and proteins. (+info)
Protective influence of vitamin E on antioxidant defense system in the blood of rats treated with cadmium.
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The effects of acute exposure to cadmium (Cd) on the blood antioxidant defense system, lipid peroxide concentration and hematological parameters, as well as the possible protective role of vitamin E were studied. Male Wistar albino rats (3 months old) were treated with cadmium (0.4 mg Cd/kg b.m., i.p., 24 h before the experiment) or with vitamin E + Cd (20 IU Vit E/kg b.m., i.m., 48 h + 0.4 mg Cd/kg b.m., i.p., 24 h before the experiment). The hematological parameters were assessed: red blood cell counts, hematocrit value and hemoglobin concentration were significantly decreased in the blood of Cd-treated rats. Intoxication with cadmium was also followed by significantly increased lipid peroxide concentrations. We also observed increased activity of antioxidant defense enzymes: copper zinc containing superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase as well as concentrations of non-enzymatic components of antioxidant defense system: reduced glutathione, vitamin C and vitamin E. Pretreatment with vitamin E exhibited a protective role on the toxic effects of cadmium on the hematological values, lipid peroxide concentration as well as on enzymatic and non-enzymatic components of antioxidant defense system. (+info)
Chronic overexposure to cadmium fumes associated with IgA mesangial glomerulonephritis.
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BACKGROUND: Cadmium is a metal used in the zinc, copper and steel industries, and in the manufacture of electric batteries and solar cells. Acute cadmium poisoning is characterized by irritation of the respiratory tract, while in chronic poisoning the main target organ is the renal tubule. AIMS: We report a patient with chronic work overexposure to cadmium, who presented a IgA mesangial glomerulonephritis with no respiratory or renal tubule involvement. Case report A 39-year-old patient was referred to our hospital for evaluation of a glomerular nephropathy. For the past 12 years he had worked as a welder, using cadmium electrodes. The patient had no respiratory symptoms and the chest X-ray was normal. Tests showed a proteinuria of 2 g in 24 h with microhaematuria [150 red blood cells/high power field (rbc/hpf)], with preservation of the renal function (creatinine clearance of 137 ml/min). The concentrations of cadmium in blood and urine were 45 micro g/l and 25 micro g/g creatinine, and an environmental study showed that levels of cadmium in the workplace were 52 micro g/m(3). A renal biopsy showed an IgA mesangial glomerulonephritis. The patient ceased to work with cadmium, and 1 year later cadmium levels had decreased and renal function was found to be stable. CONCLUSIONS: IgA mesangial glomerulonephritis is a disease of unknown aetiology which has been associated with other diseases. Chronic overexposure to cadmium may contribute to the development of this nephrophathy. (+info)
Acute study of interaction among cadmium, calcium, and zinc transport along the rat nephron in vivo.
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This study investigates the effect in rats of acute CdCl(2) (5 microM) intoxication on renal function and characterizes the transport of Ca(2+), Cd(2+), and Zn(2+) in the proximal tubule (PT), loop of Henle (LH), and terminal segments of the nephron (DT) using whole kidney clearance and nephron microinjection techniques. Acute Cd(2+) injection resulted in renal losses of Na(+), K(+), Ca(2+), Mg(2+), PO(4)(-2), and water, but the glomerular filtration rate remained stable. (45)Ca microinjections showed that Ca(2+) permeability in the DT was strongly inhibited by Cd(2+) (20 microM), Gd(3+) (100 microM), and La(3+) (1 mM), whereas nifedipine (20 microM) had no effect. (109)Cd and (65)Zn(2+) microinjections showed that each segment of nephron was permeable to these metals. In the PT, 95% of injected amounts of (109)Cd were taken up. (109)Cd fluxes were inhibited by Gd(3+) (90 microM), Co(2+) (100 microM), and Fe(2+) (100 microM) in all nephron segments. Bumetanide (50 microM) only inhibited (109)Cd fluxes in LH; Zn(2+) (50 and 500 microM) inhibited transport of (109)Cd in DT. In conclusion, these results indicate that 1) the renal effects of acute Cd(2+) intoxication are suggestive of proximal tubulopathy; 2) Cd(2+) inhibits Ca(2+) reabsorption possibly through the epithelial Ca(2+) channel in the DT, and this blockade could account for the hypercalciuria associated with Cd(2+) intoxication; 3) the PT is the major site of Cd(2+) reabsorption; 4) the paracellular pathway and DMT1 could be involved in Cd(2+) reabsorption along the LH; 5) DMT1 may be one of the major transporters of Cd(2+) in the DT; and 6) Zn(2+) is taken up along each part of the nephron and its transport in the terminal segments could occur via DMT1. (+info)
Evidence for concurrent effects of exposure to environmental cadmium and lead on hepatic CYP2A6 phenotype and renal function biomarkers in nonsmokers.
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We examined the interrelationships between phenotype of hepatic cytochrome P450 2A6 (CYP2A6), nephropathy, and exposure to cadmium and lead in a group of 118 healthy Thai men and women who had never smoked. Their urinary Cd excretion ranged from 0.05 to 2.36 microg/g creatinine, whereas their urinary Pb excretion ranged from 0.1 to 12 microg/g creatinine. Average age and Cd burden of women and men did not differ. Women, however, on average showed a 46% higher urinary Pb excretion (p < 0.001) and lower zinc status, suggested by lower average serum Zn and urinary Zn excretion compared with those in men. Cd-linked nephropathy was detected in both men and women. However, Pb-linked nephropathy was seen only in women, possibly because of higher Pb burden coupled with lower protective factors, notably of Zn (p < 0.001), in women compared with men. In men, Pb burden showed a negative association with CYP2A6 activity (adjusted beta = -0.29, p = 0.003), whereas Cd burden showed a positive association with CYP2A6 activity (adjusted beta = 0.38, p = 0.001), suggesting opposing effects of Cd and Pb on hepatic CYP2A6 phenotype. The weaker correlation between Cd burden CYP2A6 activity in women despite similarity in Cd burden between men and women is consistent with opposing effects of Pb and Cd on hepatic CYP2A6 phenotypic expression. A positive correlation between Cd-linked nephropathy (urinary N-acetyl-beta-D-glucosaminidase excretion) and CYP2A6 activity in men (r = 0.39, p = 0.002) and women (r = 0.37, p = 0.001) suggests that Cd induction of hepatic CYP2A6 expression and Cd-linked nephropathy occurred simultaneously. (+info)
The threshold cadmium level that causes a substantial increase in beta2-microglobulin in urine of general populations.
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Cadmium (Cd) is a toxic element ubiquitous in the environment, and general populations have been exposed to this element primarily via foods. Thus, the critical level of non-occupational Cd exposure to cause any health effects among general populations is of public health as well as toxicological concern. The objectives of the present study were to examine the quantitative relationship between cadmium (Cd-U) and beta2-microglobulin in urine (beta2-MG-U) as a marker of exposure to Cd and as a marker of renal tubular dysfunction, respectively, and to identify a threshold Cd-U, if present, in causing a substantial increase in beta2-MG-U. Thus, paired data on geometric mean (GM) Cd-Ucr (i.e., Cd-U as corrected for creatinine [cr] concentration) and GM beta2-MG-Ucr (beta2-MG-U as corrected for cr) of residents in polluted as well as nonpolluted areas in Japan were retrieved in international and domestic sources. In practice, 245 cases of the data pairs were obtained in 51 articles published since 1975. Statistical analysis on ordinary scales disclosed that beta2-MG-Ucr increased markedly when Cd-Ucr exceeded a certain level. The relation between the two parameters after double-logarithmic conversion was in a shape of the letter J or a stick for ice hockey. Analysis for Cd-Ucr at the flexion point gave Cd-Ucr of 4 (on double logarithmic scales) or 7 microg/g cr (on ordinary scales). Cd-Ucr levels that correspond to a beta2-MG-Ucr of 1,000 microg/g cr were estimated to be 8-9 microg/g cr, by ordinary and logarithmic assumption as well as by the 3rd degree regression analysis. Thus, it is concluded that there is a threshold Cd-Ucr level that leads to a substantial increase in beta2-MG-Ucr, and that the threshold level is greater than 4 microg/g cr. (+info)