Paradoxical increases in serum levels of highly chlorinated PCBs in aged women in clear contrast to robust decreases in dietary intakes from 1980 to 2003 in Japan.

Objective: Exposure to polychlorinated biphenyls (PCBs) is considered to have culminated between 1950 and 1970 in Japan, and exposure through diet, the major exposure route, has decreased significantly over the last 10 years. The primary goal of the present study was to investigate the long-term trends and congener profiles of serum and dietary levels of PCBs using historical samples.

Methods: Using banked samples collected in 1980, 1995, and 2003 surveys, we determined the daily intakes and serum concentrations of 13 PCB congeners (#74, #99, #118, #138, #146, #153, #156, #163, #164, #170, #180, #182, and #187) in women.

Mechanism of metal-mediated DNA damage and apoptosis induced by 6-hydroxydopamine in neuroblastoma SH-SY5Y cells.

6-Hydroxydopamine (6-OHDA) is a neurotoxin to produce an animal model of Parkinson's disease. 6-OHDA increased the formation of 8-oxo-7, 8-dihydro-2'-deoxyguanosine (8-oxodG), a biomarker of oxidatively damaged DNA, and induced apoptosis in human neuroblastoma SH-SY5Y cells. Iron or copper chelators inhibited 6-OHDA-induced 8-oxodG formation and apoptosis.

Mechanism for manganese enhancement of dopamine-induced oxidative DNA damage and neuronal cell death.

Although the cause of dopaminergic cell death in Parkinson's disease is still poorly understood, there is accumulating evidence suggesting that metal ions can be involved in the processes. We investigated the effect of manganese on cell death and DNA damage in PC12 cells treated with dopamine. Mn(II) enhanced cell death induced by dopamine.

Large-scale evaluation of the current level of polybrominated diphenyl ethers (PBDEs) in breast milk from 13 regions of Japan.

Polybrominated diphenyl ethers (PBDEs) were measured in 2004 in 105 breast milk samples collected from 13 regions of Japan (Hokkaido, Akita, Miyagi, Tokyo, Gifu, Fukui, Kyoto, Hyogo, Wakayama, Shimane, Yamaguchi, Kochi and Okinawa). Six congeners (BDE-28, BDE-47, BDE-99, BDE-100, BDE-153 and BDE-154) were determined by gas chromatography /mass spectrometry (GC/MS). Total PBDE levels ranged from 0.

Catechol and hydroquinone have different redox properties responsible for their differential DNA-damaging ability.

We examined the redox properties of the "carcinogenic" catechol and the "noncarcinogenic" hydroquinone in relation to different DNA damaging activities and carcinogenicity using 32P-labeled DNA fragments obtained from the human genes. In the presence of endogenous NADH and Cu2+, catechol induces stronger DNA damage than hydroquinone, although the magnitudes of their DNA damaging activities were reversed in the absence of NADH. In both cases, DNA damage resulted from base modification at guanine and thymine residues in addition to strand breakage induced by Cu+ and H2O2, generated during the oxidation of catechol and hydroquinone into 1,2-benzoquinone and 1,4-benzoquinone, respectively.