Impact of occupational cadmium exposure on bone in sewage workers

Cadmium (Cd) is one of the environmental risk factors for bone loss. The present study included 40 sewage workers occupationally exposed to Cd. Forty nonexposed men were included as a control group. Current smokers represented 65% and 47.5% of the exposed and control groups, respectively.

The study aimed to investigate the hazard of occupational Cd exposure on bone health. This was achieved through measuring serum and urinary Cd, and calcium (Ca), in addition to serum osteoprotegerin (OPG) and estrogen receptor-α gene. Results showed significant elevation in serum Cd, OPG, and urinary Ca levels in the exposed compared to the controls. Bony aches and joint pain were more prevalent among the exposed workers. Serum and urinary Cd increased in exposed smokers relative to control smokers. Also, serum OPG levels showed significant rise among exposed smoker and nonsmoker compared to control smoker and nonsmoker groups. Serum Cd level increased significantly in PP and pp genotypes in exposed workers compared to controls, while elevated levels of serum OPG was observed in PP and Pp genotypes in exposed workers relative to controls.

Urinary Cd exhibited significant rise in both PP and pp genotypes in exposed workers, while Ca excretion was elevated in pp genotype only. The study reflected an association of genetic predisposition and Cd exposure in progression of osteoporosis. Further research is needed to explain the mechanisms of Cd impact on bone. The role of smoking is important and hence smoking cessation programs are essential for sewage workers.     

Interactions of sulfates of divalent metals in nickel-sulfate-sensitive patients

Abstract 70 nickel-sensitive subjects who previously gave positive patch test response lto 10 μl of nickel sulfate 0.1 M, were patch tested to 10 μl of mixed aqueous solutions containing nickel sulfate 0.1 M +magnesium sulfate 0.3 M, nickel sulfale 0.1 M+zinc sulfate, 0.3 and 0.5 M, respectively, nickel sulfate 0.1 M+ manganese sulphate 0.3 and 0.5 M, respectively nickel sulphate 0.1 M+ cadmium sulfate 0.1 and 0.3 M, respectively, nickel sulfate 0.1 M + iron sulfate (III) 0.1 and 0.3 M, respectively, and to 10 μl of aq. cadmium sulfate 0.1 M, aq. cadmium sulfate 0.3 M, aq. iron sulfate 0.1 M, aq. iron sulfate 0.3 M. The results showed that, whilst sulfates of divalent metals with similar size and redox properties (Mg, Zn and Mn) were able to reduce or to suppress, in a dose-dependent way, the majority (75%) of nickel reactions, those with large radius and different oxidation state(Fe III), generally gave an increase in the reactions. In about 15% of the tested subjects, an increase in all the positive reactions to the mixed solutions was found. The findings seem to demonstrate that in only a majority but not all of nickel sulfate allergic reactions, is Ni(II) able to substitute for divalent ions with similar properties at the ion sites of some proteins. This tendency reproduces the results of experimental systems, in which nickel toxicity and cancerogenity are considered responsible. In contrast, in about 15% of the tested subjects, there was a general enhancement of the reactions. In these cases, either the occurrence of a “hyper-irritable” skin caused by the adopted test system or, more likely, the formation of Ni complexes with different geometries, is hypothesized.     

硒、镉的摄入对大鼠肝细胞器膜元素分布的影响

用扫描电镜Ｘ线能谱仪分析肝细胞器膜元素构成成分和磷硫做参比的相对含量变化，并结合原子吸收法测定肝组织Ｚｎ、Ｃｕ、Ｓｅ、Ｃｄ含量进行对比，观察Ｗｉｓｔａｒ大鼠分别摄入硒（５ｍｇ／Ｌ）、镉（５０ｍｇ／Ｌ）和硒镉（５ｍｇ／Ｌ＋５０ｍｇ／Ｌ）３周后肝细胞器膜元素分布的影响。结果显示：肝细胞器膜的构成元素主要有两种，一种是以含硒为主，经Ｃｄ处理后其Ｃａ、Ｚｎ含量比其它处理组增加更为明显；另一种则以Ｚｎ、Ｃｕ为主，其铜百分值及锌铜百分含量之和以镉组下降最多。膜上各元素峰值的硫磷比值结果为：镉组Ｆｅ、Ｃｄ上升较明显，Ｚｎ以硒镉组上升最甚，Ｃｕ以硒和硒镉组上升较明显。各处理组肝组织Ｃｄ、Ｚｎ含量均有显著性上升，与膜上元素变化趋于一致。     

The toxicity and bioaccumulation of cadmium and copper as affected by humic acid

The toxicity of Cd and Cu to daphnids was evaluated over a 42-day exposure period at three humic acid concentrations. The addition of humic acid to test water decreased the acute and chronic toxicity of Cu but increased the acute and chronic toxicity of Cd. However, there was no effect of HA on the bioaccumulation of either metal. At the highest concentration, the presence of humic acid actually resulted in an increase in mean brood sizes of Cu-exposed animals and prevented a reduction in mean brood sizes of Cd-exposed animals.     

Characterization of the proteinuria induced by prolonged oral administration of cadmium in female rats

Female Sprague-Dawley rats were given 200 ppm cadmium (Cd) in the drinking water for 11 months. Total proteinuria and the concentrations of Cd in blood, urine, liver and kidney cortex were determined monthly. The proteinuria was characterized by Sephadex G-75 chromatography and by sodium dodecyl sulfate-polyacrylamide gel electrophoresis.

From the 8th month of treatment, the Cd concentration in the kidney cortex levels off at a value of about 250 μg/g wet wt and this phenomenon coincides with the occurrece of proteinuria. The proteinuria was characterized by an increased urinary excretion of high molecular weight (HMW) proteins, particularly γ-globulins. Aminoaciduria also increased which suggests the existence of a slight tubular dysfunction. The renal dysfunction induced by chronic oral administration of Cd seems different from that observed in a previous study in which Cd was administered by the i.p. route (1 mg Cd/kg, 5 times a week for 2 months). For the same level of Cd in the kidney cortex the proteinuria induced by i.p. injection of Cd was usually of mixed type and in some cases of the tubular type. The development of this proteinuria was coincident with the levelling off of Cd concentration in the kidney cortex and in the liver. The saturation of liver by Cd is very likely at the origin of the extensive tubular lesion and of the mixed type proteinuria observed in the i.p. experiment. These results demonstrate the importance of the mode of Cd administration on the nature of the Cd-induced proteinuria in animal. They support also our proposal that both low and HMW proteins should be determined in urine for the early detection of renal damage occurring in man chronically exposed to cadmium.     

Projections of the zona incerta in the cat, with stimulation controls.

In eight cats single electrolytic lesions were placed in the zona incerta, and resultant fiber degeneration studies were made. In seven additional cats, stimulating electrodes were chronically implanted bilaterally into the zona incerta, H₂ (lenticular fasciculus), or H (prerubral) fields of Forel. The animals were placed in a two-compartment shuttle box, and a routinely established procedure of subthalamic stimulation was instituted. When the sensory (nociceptive) or motor manifestations and reactions were established, small lesions were made through both poles of the electrodes. The brains were studied by silver techniques for degenerating axons and terminals. Findings in the latter group of animals with physiologic substrates, compared to those in the first group, indicated that the zona incerta contains at least two major physiologic-anatomic components with differential fiber projections. The first component is a medial zona incerta proper or caudalis, paleospinothalamic, nociceptive-conducting system which causes typical escape responses. Its unequivocal projections are to the nucleus of the H₁ field, posterior and dorsal hypothalamus, part of the intralaminar system, ventromedial and ventralis anterior nuclei, nucleus reuniens, reticular nucleus, pulvinar, posterior nucleus, central gray, red nucleus, and the central tegmental tract. The second constitutent concerns pyramidal-extrapyramidal motor type responses that arise with avoidance reactions from other portions of the zona incerta. In these cases there is heavy projection to the caudate, entopenduncular, globus pallidus, and putamen nuclei. In contrast, degeneration from the nociceptive part of the zona incerta or H₂ and H fields to these nuclei is minimal.     

Zinc and cadmium in cell fractions of prostatic cancer tissues of different histological grading in comparsion to BPH and normal prostate

Summary The concentrations of zinc and cadmium in cellular fractions of normal prostate gland, BPH and prostatic carcinomas of different histological grading were determined by electrothermal atomic absorption spectrometry. We found distinct differences in the content of Zn and Cd in the nuclear fractions of malignant tissues in comparison with BPH and normal prostatic tissues. The highest values of Cd were obtained in the nuclear fractions of poorly-differentiated carcinomas. In these samples we also found a low concentration of zinc. In comparison to this the highest Zn-values were found in the nuclear fraction of the BPH.     

Diabetic microangiopathy. I. Current status of the chemistry and metabolism of the glomerular basement membrane.

In recent years, the nature of the renal glomerular basement membrane has been the subject of numerous investigations. In diabetes mellitus, the renal glomerulus is characterized primarily by thickening of the basement membrane and excessive accumulation of basement membrane-like material in the mesangial region. Compositional analyses have shown that basement membranes are glycoprotein in nature. Studies of the glomerular basement membranes in diabetes have indicated a change from normal chemical composition. Furthermore, studies of the metabolism of diabetic kidneys in experimental animals, using cortical homogenates and isolated glomeruli, have demonstrated higher anabolic and lower catabolic enzyme activities. However, contradictory data have been reported with regard to both the chemical composition and metabolism of the kidney in human and experimental diabetes. This review attempts to examine these reports in detail and discuss the possible causes for these discrepancies.     

Chromosome changes in human lymphocytes after separate and combined treatment with divalent salts of lead,cadmium, and zinc

Unstimulated human lymphocytes in whole blood were treated for three hours with lead, cadmium, and zinc acetate separately and in combinations of two or three metal salts with different concentrations of between 10^?3 and 10^?8 moles, respectively. Untreated cultures and sodium acetate-treated samples served as controls. Chromosome analysis from 48 cultures revealed higher incidences of chromatid-type aberrations and gaps only for cultures exclusively treated with cadmium. The results are discussed under the aspect of heavy metal metabolism in human lymphocytes.     

Evidence for induced microsomal bilirubin degradation by cytochrome P450 2A5

Oxidative metabolism of bilirubin (BR) -- a breakdown product of haem with cytoprotective and toxic properties -- is an important route of detoxification in addition to glucuronidation. The major enzyme(s) involved in this oxidative degradation are not known. In this paper, we present evidence for a major role of the hepatic cytochrome P450 2A5 (Cyp2a5) in BR degradation during cadmium intoxication, where the BR levels are elevated following induction of haem oxygenase-1 (HO-1). Treatment of DBA/2J mice with CdCl(2) induced both the Cyp2a5 and HO-1, and increased the microsomal BR degradation activity. By contrast, the total cytochrome P450 (CYP) content and the expression of Cyp1a2 were down-regulated by the treatment. The induction of the HO-1 and Cyp2a5 was substantial at the mRNA, protein and enzyme activity levels. In each case, the up-regulation of HO-1 preceded that of Cyp2a5 with a 5-10h interval. BR totally inhibited the microsomal Cyp2a5-dependent coumarin hydroxylase activity, with an IC(50) approximately equal to the substrate concentration. The 7-methoxyresorufin 7-O-demethylase (MROD) activity, catalyzed mainly by the Cyp1a2, was inhibited up to 36% by BR. The microsomal BR degradation was inhibited by coumarin and a monoclonal antibody against the Cyp2a5 by about 90%. Furthermore, 7-methoxyresorufin, a substrate for the Cyp1a2, inhibited BR degradation activity by approximately 20%. In sum, the results strongly suggest a major role for Cyp2a5 in the oxidative degradation of BR. Secondly, the coordinated up-regulation of the HO-1 and Cyp2a5 during Cd-mediated injury implicates a network of enzyme systems in the maintenance of balancing BR production and elimination.