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Tuder R.M.,Aurora University | Yoshida T.,Institute of Environmental Toxicology
Proceedings of the American Thoracic Society | Year: 2011

The maintenance of the alveolar structure is required throughout life. To accomplish this goal, alveolar cells, including endothelial, epithelial, and fibroblastic cells, provide key molecules with broad survival and antiapoptotic effects. These complex interactions are disrupted by cigarette smoke, leading to emphysema. Smoke imposes an environmental stress to the lung with the activation of "sensor-like" molecular signaling. Activation of RTP801, leading to mTOR inhibition, is paradigmatic of these responses. The accumulation of cellular damage, with the generation of endogenous mediators of inflammation, may proceed toward an aging phenotype. These alterations may impose significant challenges to cell-based regenerative or pharmacological therapies. Source


Satsuma K.,Institute of Environmental Toxicology
Applied Microbiology and Biotechnology | Year: 2010

A novel s-triazine-mineralizing bacterium-Nocardioides sp. strain DN36-was isolated from paddy field soil treated with ring-U-14C-labeled simetryn ([14C]simetryn) in a model paddy ecosystem (microcosm). In a tenfold-diluted R2A medium, strain DN36 liberated 14CO2 from not only [14C]simetryn but also three ring-U- 14C-labeled s-triazines: atrazine, simazine, and propazine. We found that DN36 mineralized ring-U-14C-cyanuric acid added as an initial substrate, indicating that the bacterium mineralized s-triazine herbicides via a common metabolite, namely, cyanuric acid. Strain DN36 harbored a set of genes encoding previously reported s-triazine-degrading enzymes (TrzN-AtzB-AtzC), and it also transformed ametryn, prometryn, dimethametryn, atraton, simeton, and prometon. The findings suggest that strain DN36 can mineralize a diverse range of s-triazine herbicides. To our knowledge, strain DN36 is the first Nocardioides strain that can individually mineralize s-triazine herbicides via the ring cleavage of cyanuric acid. Further, DN36 could not grow on cyanuric acid, and the degradation seemed to occur cometabolically. © 2010 Springer-Verlag. Source


The Developmental Neurotoxicology (DNT) Committee has been working to promote developmental neurotoxicology and related scientific areas of interest to integrate academic and regulatory sciences in this field since the Behavioral Teratology Meeting was established by the Japanese Teratology Society in 1982. The committee has led several large-scale collaborative studies to standardize existing methodologies and held symposiums and workshops periodically at the society's annual meetings. This overview provides a history of the DNT Committee, as well as a brief summary of the DNT Symposium in 2011. © 2012 Japanese Teratology Society. Source


Aoyama H.,Institute of Environmental Toxicology | Chapin R.E.,Pfizer
Vitamins and Hormones | Year: 2014

Methoxychlor is an organochlorine pesticide having a weak estrogenicity, which is estimated to be approximately 1000- to 14,000-fold less potent to a natural ligand, 17β-estradiol. However, its active metabolite, hydroxyphenyltrichloroethane, has much more potent estrogenic activity and probably acts in the target organs of animals exposed to methoxychlor at least 100 times stronger than the parent compound. A variety of in vivo reproductive toxicity studies have shown that treatment with methoxychlor exerts typical endocrine-disrupting effects manifest as estrogenic effects, such as formation of cystic ovaries resulting in ovulation failures, uterine hypertrophy, hormonal imbalances, atrophy of male sexual organs, and deteriorations of sperm production in rats and/or mice, through which it causes serious reproductive damages in both sexes of animals at sufficient dose levels. However, methoxychlor is not teratogenic. The no-observed-adverse-effect level of methoxychlor among reliable experimental animal studies in terms of the reproductive toxicity is 10. ppm (equivalent to 0.600. mg/kg/day) in a two-generation reproduction toxicity study. © 2014 Elsevier Inc. Source


Gotoh H.,Institute of Environmental Toxicology | Aoyama H.,Institute of Environmental Toxicology
Congenital Anomalies | Year: 2012

Genetic disorders are usually considered to be caused by harmful gene mutations, as well as by chromosomal aberrations, including small insertions, duplications and/or deletions. However, as infertile individuals often arise among the offspring of crosses between two fertile mouse strains, we postulate that a certain combination of 'normal' genes with neither gene mutations nor chromosomal aberrations can cause such serious phenotypic alterations as reproductive dysfunction. In this study, we show evidence that a combination of multiple normal genes from two different normal mouse strains manifests a wide range of male reproductive dysfunctions, from benign changes to complete infertility. These abnormal phenotypes are thought to have occurred by epistatic interactions of alleles. © 2012 The Authors. Congenital Anomalies © 2012 Japanese Teratology Society. Source

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