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No abstract available. [ABSTRACT FROM AUTHOR]

Forty-eight human milk samples were collected from primiparous mothers in Osaka City from June 1999 to January 2000 and analyzed for polychlorinated dibenzo- p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and dioxin-like coplanar polychlorinated biphenyls (CoPCBs). Mean toxic equivalents (TEQs) in the milk were 13.86 pg I-TEQ/g fat or 16.50 pg World Health Organization (WHO)-TEQ/g fat for PCDDs and PCDFs; 9.87 pg WHO-TEQ/g fat for CoPCBs; and 23.74 pg TEQ/g fat using I-TEQ values of PCDDs and PCDFs or 26.36 pg TEQ/g fat using WHO-TEQ values of PCDDs and PCDFs for total PCDDs, PCDFs, and CoPCBs. The TEQ levels of these chemicals in human milk in Osaka City were in the range of levels in human milk surveyed in Japan, but the TEQ levels of PCDDs and PCDFs and total PCDDs, PCDFs, and CoPCBs from our study were slightly higher than average TEQ levels in human milk in Japan. When comparing our data with the latest data from the United States and some European countries, the TEQ levels of PCDDs and PCDFs in human milk from Osaka City were relatively high, whereas those of CoPCBs were ranked as being of intermediate level. Only TEQ values of CoPCBs in human milk were found to correlate with the increasing age of mothers and their estimated intake of seafood during the year before pregnancy. Concentrations of PCBs 105 and 118 contributed to TEQ values of CoPCBs associated with seafood intake, whereas those of PCBs 156, 157, 114, 189, 167, and 169 contributed to TEQ values of CoPCBs associated with increasing maternal age. [ABSTRACT FROM AUTHOR]

Investigates the effects of cysteine on the cytotoxicity of arsenic compounds, such as arsenite, arsenate, methylarsonic acid, and dimethylarsinic acid, in cultured human HL-60 cells. Rank order of the mixtures of arsenicals with cysteine; Possible role of the trivalent arsenic in the mixtures of arsenicals with cysteine in enhanced cytotoxicity and apoptosis.

Using a newly identified organomercury lyase gene (merB3) expression system from TnMERI1, the mercury resistance transposon first found in Gram-positive bacteria, a dual-purpose system to detect and remove organomercurial contamination was developed. A plasmid was constructed by fusing the promoterless luxAB genes as bioluminescence reporter genes downstream of the merB3 gene and its operator/promoter region. Another plasmid, encoding mer operon genes from merR1 to merA, was also constructed to generate an expression regulatory protein, MerR1, and a mercury reductase enzyme, MerA. These two plasmids were transformed into Escherichia coli cells to produce a biological system that can detect and remove environmental organomercury contamination. Organomercurial compounds, such as neurotoxic methylmercury at nanomolar levels, were detected using the biomonitoring system within a few minutes and were removed during the next few hours. [ABSTRACT FROM AUTHOR]

Postoperative recovery of patients with chronic subdural haematoma (CSH) was investigated by comparing pre- and postoperative coagulant and fibrinolytic activity in the haematoma contents of 15 patients with SCH. Patients in this study were treated draining the haematoma cavity without irrigation, a procedure dubbed the closed drainage. Haematomas were collected during, and 24 hrs after, surgery. Postoperative fibrinolytic activity was lower than that observed pre-operatively. In particular, levels of tissue plasminogen activator activity (TPA), and fibrin and fibrinogen degradation products (FDP) all decreased. In contrast, coagulant activity increased postoperatively. This paper will discuss the role of local coagulofibrinolysis in the postoperative recovery of CSH patients. [ABSTRACT FROM AUTHOR]

The article presents a study which examines the acute toxic effect of water from River Yodo, Japan on Daphnia magna or D. magna. The study involved river-water sampling and analysis to examine and detect the acute toxic effect of River Yodo water. Results show that insecticides are the main toxicants to D. magna.

The biotransformation following oral administration of dimethylarsinic acid (DMA), an organoarsenical herbicide and the main metabolite of inorganic arsenic in mammals, was studied in rats. Male F344/DuCrj rats were administered a single dose of DMA (50 mg/kg) orally. Urine was collected at 0, 2, 4, 8, 10, 24, and 48 h after administration byforced urination. Arsenic metabolites in urine were analyzed by ion chromatography with inductively coupled plasma mass spectrometry (IC-ICP-MS). The proportions of urinary elimination of DMA, trimethylarsine oxide (TMAO), methylarsonic acid (MMA), an unidentified arsenic metabolite, and arsenite were determined at various timepoints after administration. Unmetabolized DMA was the most common form excreted during the first 4 h. Thereafter, a gradual decrease in the proportion of DMA was observed, while progressive increases in those of TMAO, theunidentified metabolite, and arsenite occurred. The proportion of TMAO excreted amounted to over 50% of all arsenic in urine between 6 and 24 h. The proportion of the unidentified metabolite and arsenite were each approximately 10% at 10 and 24 h after administration. The findings indicate that DMA administered to rats was initially excreted as unchanged DMA, and later as the methylated metabolite, TMAO. Arsenite, a demethylated metabolite of DMA, also was excreted later than elimination of DMA and TMAO. The hypothesis of demethylation by intestinal microorganisms can be supported by comparing the metabolites following oral and intraperitoneal administration. The unidentified metabolite was readily decomposed by HCl but was left unchanged by NaOH; these findings suggest that it was present in a complexed form in urine. [ABSTRACT FROM AUTHOR]

The toxic effects of arsenic compounds on cell division were studied, using Chinese hamster V79 cells. Seven arsenic compounds were tested. Inorganic arsenic compounds (arsenite and arsenate), which have been found in drinking water, inhibited cell growth at very low concentrations. Monomethylarsonic acid (MMA), dimethylarsinic acid (DMA), and trimethylarsine oxide (TMAO), which are methylated metabolites of inorganic arsenics, were less cytotoxic than the inorganic arsenics themselves. The cytotoxicity of the three methylated metabolites decreased as the number of methyl groups increased. Arsenobetaine (AsBe) and arsenocholine (AsC), which have been found in some marine products,did not show any cytotoxicity. Three methylated metabolites; MMA, DMA and TMAO induced mitotic arrest. Tetraploidy production was observed in cells exposed to DMA or TMAO. Arsenite, arsenate, AsBe and AsC did not induce mitotic arrest or tetraploids. These results suggest that MMA, DMA and TMAO exert some effect on cell division in metaphase and may thereby give some clue as to the carcinogenic mechanism of arsenic. [ABSTRACT FROM AUTHOR]