摘要:

In order to elucidate whether urinary levels of inorganic and organic arsenic metabolites are associated with previous exposure to high-arsenic artesian well water, a total of 302 residents of age 30 yr or older were recruited from three arseniasis-hyperendemic villages in Taiwan. Most study subjects had stopped consuming high-arsenic artesian well water for more than 20 yr. The mean total arsenic (Ast) determined by inductively cout pled plasma mass spectrometer (ICPMS) was 267.05 +/- 20.95 mug/L, and the mean level of inorganic arsenic and its metabolites (Ast) was 86.08 +/- 3.43 mug/L. In the multivariate analysis, urinary dimethylarsinic acid (DMA) levels were significantly inversely associated with age, with women exhibiting significantly lower urinary amounts of arsenite [As(III)], arsenate [As(V)], monomethylarsonic acid (MMA), organic arsenic (Aso), and Ast compared to men. After adjustment for age and sex, previous cumulative arsenic exposure through consumption of artesian well water was significantly associated with elevated urinary levels of MMA and DMA, but not As(III) + As(V), Asot, and Ast. In the multivariate analysis, the percentage of As in As was significantly higher in men than women, but this was not significantly associated with age. The percentage of As(III) + As(V) in As increased significantly with age, while the reverse was noted with DMA in Asi. Women had a significantly higher DMA percentage but lower As(III) + As(V) and MMA percentages in Asi than men. After adjustment for age and sex, the percentages of As(III) + As(V) in Asi were significantly inversely associated with previous arsenic exposure through consumption of artesian well water. Data suggested that women seem to possess a more efficient arsenic methylation capability than men, and aging diminishes this methylation capability; furthermore, the higher the cumulative arsenic exposure, the greater is the body burden of inorganic arsenic, mainly in the form of MMA and DMA.

ISSN:1528-7394    

DOI:10.1080/009841098158728

出版商:Informa UK Ltd    

年代:1998

数据来源: Taylor

摘要:

Metallothioneins (MT) are ubiquitous, low-molecular-weight proteins that exhibit high binding affinities for heavy metal ions. The expression of these cysteine-rich proteins is induced in response to various types of chemical and physical stresses and therefore can be used to assess human exposure to cytotoxic environmental agents. In the current study, MT levels of human peripheral blood lymphocytes were determined using an MT-specific antibody and flow cytometry. Treatment of human whole blood ex vivo with CdCl2 was found to induce a concentration- and time-dependent increase in lymphocyte MT levels at concentrations as low as 0.3 mu M and within a 12-h period. Interestingly, differences were observed in the magnitude of cadmium-induced MT levels in the lymphocytes of six human test subjects. Two members of the study population exhibited CdCl2-induced cellular MT levels that were up to twofold greater than the lymphocytes of other human subjects. While the lymphocytes of most test subjects exhibited a symmetric (unimodal) distribution of cadmium-induced MT-specific fluorescence, the cells of two individuals displayed a heterogeneous (nonuniform) distribution of MT levels. Dual-parameter flow cytometric analysis using phenotype-specific antibodies indicated that variations in the responsiveness of subpopulations of lymphocytes to CdCl2 were responsible for the heterogeneous distribution of MT-specific cellular fluorescence. Thelper (CD4-positive) and T-suppressor/cytotoxic (CD8-positive) lymphocytes expressed higher cellular levels of MT than other lymphocyte subpopulations (i.e., B lymphocytes, natural killer cells). Our results suggest that MT protein levels of peripheral blood lymphocytes, as determined by this flow cytometric method, may be used to assess human exposure to toxic metals and to characterize various quantitative/qualitative aspects of the response of individuals to cadmium and possibly to other types of environmental stresses.

ISSN:1528-7394    

DOI:10.1080/009841098158737

出版商:Informa UK Ltd    

年代:1998

数据来源: Taylor

摘要:

The use of pesticides in agriculture has increased over the last decade. Their widespread, often uncontrolled use causes thousands of people to be daily exposed to environmental agricultural chemicals, resulting in acute and chronic health effects. At present there is a paucity of data on the potential adverse effects of exposure to low levels of mancozeb for prolonged periods. In order to investigate the effects of mancozeb exposure on pulmonary wildlife populations, tracheas and lungs of nine 1- to 7- yr-old nonmigratory pigeons raised near peach orchards and vineyards repeatedly sprayed with the fungicide were examined. The experimental situation allowed us to evaluate the long-term natural toxicity of mancozeb as a sentinel for human populations occupationally exposed to fungicides. The use of nonmigratory pigeons may serve as an important biological source from which helpful data may be obtained for assessing risks to human health and gaining new insight into pathogenetic mechanisms.

ISSN:1528-7394    

DOI:10.1080/009841098158746

出版商:Informa UK Ltd    

年代:1998

数据来源: Taylor

摘要:

Prolonged hyperglycemia results in a number of diabetic complications, including retinopathy. Pericyte degeneration is one of the earliest histological changes observed in the development of diabetic retinopathy. Increased free radicals generated under hyperglycemia could damage the retina, which abounds in polyunsaturated fatty acids. In the current study, a severalfold increase in thiobarbituric acid-reactive substances was found in rat retina cultured in hyperglycemic medium, which decreased significantly when trolox, an amphipathic antioxidant, was included in the medium. To examine the contribution of oxidative stress in vivo, diabetic rats were fed trolox ( 0.4% in the diet) during the course of the experiments. After 5 mo of hyperglycemia, whole mounts of retinal vessels were prepared and endothelial cells ( E) and pericytes (P) were counted. The ratio of E/P in the retinas obtained from normal rats, diabetic rats, and diabetic rats fed trolox were 1.74 +/- 0.186, 3.78 +/- 0.47, and 2.32 +/- 0.24, respectively. A significant restoration of pericytes by trolox suggests the involvement of oxidative injury during pericyte loss in diabetic retinopathy.

ISSN:1528-7394    

DOI:10.1080/009841098158755

出版商:Informa UK Ltd    

年代:1998

数据来源: Taylor

摘要:

Kashin-Beck disease (KBD) , an endemic, chronic osteoarthritic disorder with necrosis of chondrocytes, commonly occurs in China. The humic substance present in the drinking water of endemic areas has been proposed as one of the causative factors. In this study an in vitro cell culture system was used to investigate the damaging effects of humic acid (HA), a constituent of humic substance, on cultured rabbit articular chondrocytes. The commercial Aldrich humic acid (AHA) was fractionated with a series of organic solvents including n -hexane, benzene, ethyl acetate, and methanol. Among the several fractions of AHA, the ethyl acetate fraction (AHA-[EA]) displayed the most potent inhibitory effect on the survival of chondrocytes in clonogenic assays. Cellular injury induced by AHA-[EA] was evaluated by measuring cell viability with methylthiazol tetrazolium (MTT) and by determining the release of intracellular lactate dehydrogenase (LDH). Incubation of chondrocytes with AHA-[EA] (100-500 mug/ml) for 12 h produced a concentration-dependent decrease in cell viability and increase in LDH release. In addition, AHA-[EA] triggered lipid peroxidation manifested by elevated malondialdehyde (MDA) formation. In chemiluminescence assay, AHA-[EA] at the concentrations of 150-600 mug/ ml caused 6- to 15-fold increases of luminol-amplified chemiluminescence responses, which are considered to reflect the production of hydrogen peroxide (H2O2). Moreover, pretreating the cells with 500-750 U/ml of catalase significantly prevented the loss of cell viability, while superoxide dismutase (SOD) enhanced the adverse effect of 300 mug/ml AHA-[EA]. Data suggest that the injury to chondrocytes induced by AHA[EA] may be first through O2 production, which is then converted into H2O2, thus initiating lipid peroxidation and leading to chondronecrosis observed in KBD.

ISSN:1528-7394    

DOI:10.1080/009841098158764

出版商:Informa UK Ltd    

年代:1998

数据来源: Taylor

摘要:

The biochemical effects of hydrogen sulfide were investigated by treating enzyme homogenates and synaptosomes prepared from mammalian brain with sodium sulfide. Brain cytochrome c oxidase activity was highly sensitive to inhibition by sodium sulfide, as demonstrated by an IC50 of 0.13 muM. Sodium sulfide was also found to inhibit carbonic anhydrase activity in cerebellum, frontal cortex, and hippocampus. Synaptosomal oxygen consumption was significantly reduced as the concentration of sodium sulfide was increased from 20 to 100 muM; this was accompanied by a concentration-dependent depolarization of the synaptosomal mitochondrial membrane in situ and a reduction in synaptosomal ATP concentration. In other experiments using synaptosomes, sodium sulfide caused a significant calcium-independent increase in the extracellular accumulation of L-glutamate, inhibited Na+-dependent uptake of [3H]glutamate, but was unable to influence intrasynaptosomal free ionic Ca2+. Parallel studies conducted in vivo showed that rats exposed over a 5-d period to hydrogen sulfide (100 ppm for 3 h/d) had significantly higher concentrations of L-glutamate in the hippocampus compared to control animals. In summary, our results indicate that sulfide causes extensive disruption to respiratory and related mitochondrial functions in mammalian brain in vitro. The reduced capacity of nerve endings to take up L-glutamate may contribute to the raised L-glutamate levels observed in vivo.

ISSN:1528-7394    

DOI:10.1080/009841098158773

出版商:Informa UK Ltd    

年代:1998

数据来源: Taylor