Despite numerous applications, the cellular-clearance mechanism of multiwalled carbon nanotubes (MWCNTs) has not been clearly established yet. Previous in vitro studies showed the ability of oxidative enzymes to induce nanotube degradation. Interestingly, these enzymes have the common capacity to produce reactive oxygen species (ROS). Here, we combined material and life science approaches for revealing an intracellular way taken by macrophages to degrade carbon nanotubes. We report the in situ monitoring of ROS-mediated MWCNT degradation by liquid-cell transmission electron microscopy. Two degradation mechanisms induced by hydroxyl radicals were extracted from these unseen dynamic nanoscale investigations: a non-site-specific thinning process of the walls and a site-specific transversal drilling process on pre-existing defects of nanotubes. Remarkably, similar ROS-induced structural injuries were observed on MWCNTs after aging into macrophages from 1 to 7 days. Beside unraveling oxidative transformations of MWCNT structure, we elucidated an important, albeit not exclusive, biological pathway for MWCNT degradation in macrophages, involving NOX2 complex activation, superoxide production, and hydroxyl radical attack, which highlights the critical role of oxidative stress in cellular processing of MWCNTs.

Maternal fish consumption brings both risks and benefits to the fetus from the standpoint of methylmercury (MeHg) and n-3 PUFA (polyunsaturated fatty acids). MeHg is one of the most risky substances to come through fish consumption, and mercury concentrations in red blood cells (RBC-Hg) are the best biomarker of MeHg exposure. Docosahexaenoic acid (DHA, C22:6n-3), which is one of the most important fatty acids for normal brain development and function, is also derived from fish consumption. Our objective in this study was to examine the relationships between RBC-Hg and plasma fatty acid composition in mother and fetus at parturition. Venous blood samples were collected from 63 pairs of mothers and fetuses (umbilical cord blood) at delivery. In all cases, fetal RBC-Hg levels were higher than maternal RBC-Hg levels. The geometric mean of fetal RBC-Hg was 13.4 ng/g, which was significantly (p < 0.01) higher than that of maternal RBC-Hg (8.41 ng/g). While the average fetal/maternal RBC-Hg ratio was 1.6, the individual ratios varied from 1.08 to 2.19, suggesting considerable individual differences in MeHg concentrations between maternal and fetal circulations at delivery. A significant correlation was observed between maternal and fetal DHA concentrations (r = 0.37, p < 0.01). Further, a significant correlation was observed between RBC-Hg and plasma DHA in fetus (r = 0.35, p < 0.01). These results confirm that both MeHg and DHA which originated from fish consumption transferred from maternal to fetal circulation and existed in the fetal circulation with a positive correlation. Pregnant women in particular need not give up eating fish to obtain such benefits. However, they would do well to at least consume smaller fish, which contain less MeHg, thereby balancing the risks and benefits from fish comsumption.

It is suggested that Japanese children may ingest similar doses per body weight of methylmercury to their mothers. If maternal hair mercury was used as a proxy for mercury exposure at birth, no significant dose-effect associations with the BAEP latencies were observed in Japanese children with exposure levels below 6.9 mug/g of hair mercury, but only when higher-level exposures from Madeiran children were included. The BMDL was lower for the merged data than for Madeiran children alone.

Despite the potential limitations involved in the retrospective study, these findings suggest that prenatal methylmercury exposure (median of estimated maternal hair mercury at parturition, 2.24 microg/g) may be associated with reduced parasympathetic activity and/or sympathovagal shift.

Objectives: Exposure misclassification is a major obstacle to obtain accurate dose-response relationships. In order to solve this problem, the impact of hair treatment on total mercury in hair was assessed in Japanese women.Methods: A cross-sectional study was carried out among 327 women at age 24-49 years to determine hair mercury levels and estimate daily mercury intakes from seafood by using a food frequency questionnaire.Results: Hair mercury levels in the women and daily mercury intake ranged from 0.11 to 6.86 (median 1.63) μg/g and from 0.77 to 144.9 (median 15.0) μg/day, respectively. The hair mercury was positively correlated with the daily mercury intake (p<0.001). When the women were divided into two subgroups based on artificial hair-waving, hair coloring/dyeing, residence (non-fishing and fishing areas), and working status, a significant difference in the hair mercury level was observed between the women with and without artificial hair-waving only (p<0.001). The multiple regression analysis showed that the log-transformed hair mercury level was significantly related to the log-transformed daily mercury intake (standardized regression coefficient βs=0.307) and artificial hair-waving (βs=−0.276); but not to hair coloring/dyeing, residence, working status or age. Permanent hair treatment was estimated to reduce total mercury in hair by approximately 30%, after adjusting for daily mercury intake and other possible factors.Conclusions: These findings suggest that hair mercury is not the best biomarker of methylmercury exposure when a study population includes women with artificial hair-waving.

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In this article, we proposed a negative selection algorithm which based on hierarchical level cluster of self dataset CB-RNSA. First the self data set is clustered by different cluster radius, and then the self data are substituted by cluster centers to compare with candidate detectors to reduce the number of distance counting. In the detector creating process, the value of each detector property was restricted to a given value range so as to decrease the redundancy of detectors. The stimulation result shows that CB-RNSA is an effective algorithm for the creation of artificial immune detectors.

This paper describes the deficits in brain regional growth of rats treated with methylmercury (MeHg) among the postnatal developing phases. Rats were orally administered 10 mg/kg/day of methylmercury chloride (MMC) for 10 consecutive days from postnatal days 1 (PD-1), -14 and -35, which corresponded to the early-, late-and postbrain growth spurt, respectively. Weight-matched control rats were periodically isolated from their mother or diet and placed in an incubator for intervals of 4 to 10 hr in order to adjust the body weight to MMC-treated rats. The earlier the postnatal phase the higher the resistance to body weight loss induced by MMC. The rats were dissected on the day after final MMC treatment and the weight of organs and their mercury (Hg) concentrations were measured. Hg accumulation in the brain on the day after final treatment with 10 mg/kg/day of MMC was highest in the rats treated during the late-brain growth spurt. On the other hand, Hg accumulations in the liver and kidney increased rapidly with development of postnatal phases. Then, the brain/kidney and brain/liver ratio of Hg concentration were much higher in early postnatal rats than in later one. The weight of brain regions in MMC-treated rats was compared with those in weight-matched control rats. The significantly lower weight of the cerebrum, cerebellum and midbrain + diencephalon were confirmed in rats treated with MMC during the early-brain growth spurt. The significantly lower cerebellum weight was confirmed in rats treated with MMC during the late-brain growth spurt. The Significant differences were not observed in the brain regions in rats treated during post-brain growth spurt. In the case of human, a similar reduction of the brain weight occurred in the fetal and non-fetal infantile Minamata disease patients. The experiment using postnatal rats succeeded to reproduce the deficit in the brain growth during the earlyand late brain growth spurt by MMC treatment.