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Dive into the research topics where Seiji Kodama is active.

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Featured researches published by Seiji Kodama.


Oncogene | 2003

Radiation-induced DNA damage and delayed induced genomic instability

Keiji Suzuki; Mitsuaki Ojima; Seiji Kodama; Masami Watanabe

Ionizing radiation induces genomic instability, which is transmitted over many generations after irradiation through the progeny of surviving cells. Induced genomic instability is manifested as the expression of the following delayed effects: delayed reproductive death or lethal mutation, chromosomal instability, and mutagenesis. Since induced genomic instability accumulates gene mutations (actually genomic instability is the process whereby gene mutation increases subtle difference) and gross chromosomal rearrangements, it has been thought to play a role in radiation-induced carcinogenesis. Radiation-induced genomic instability exerts its effects for prolonged periods of time, suggesting the presence of a mechanism by which the initial DNA damage in the surviving cells is memorized. Recent studies have shown that such memory transmission causes delayed DNA breakage, which in turn plays a role in the induction of delayed phenotypes. Although radiation-induced genomic instability has been studied for years, many questions remain to be answered. This review summarizes the current data on radiation-induced genomic instability. In particular, the mechanism(s) involved in the initiation and perpetuation of radiation-induced genomic instability, and a role of delayed activation of p53 protein are discussed.


Free Radical Biology and Medicine | 2003

Relief of oxidative stress by ascorbic acid delays cellular senescence of normal human and Werner syndrome fibroblast cells

Genro Kashino; Seiji Kodama; Yukiko Nakayama; Keiji Suzuki; Kazuaki Fukase; Makoto Goto; Masami Watanabe

Primary human cells have a definite life span and enter into cellular senescence before ceasing cell growth. Oxidative stress produced by aerobic metabolism has been shown to accelerate cellular senescence. Here, we demonstrated that ascorbic acid, used as an antioxygenic reagent, delayed cellular senescence in a continuous culture of normal human embryonic cells, human adult skin fibroblast cells, and Werner syndrome (WS) cells. The results using human embryonic cells showed that treatment with ascorbic acid phospholic ester magnesium salt (APM) decreased the level of oxidative stress, and extended the replicative life span. The effect of APM to extend the replicative life span was also shown in normal human adult cells and WS cells. To understand the mechanism of extension of cellular life span, we determined the telomere lengths of human embryonic cells, both with and without APM treatment, and demonstrated that APM treatment reduced the rate of telomere shortening. The present results indicate that constitutive oxidative stress plays a role in determining the replicative life span and that suppression of oxidative stress by an antioxidative agent, APM, extends the replicative life span by reducing the rate of telomere shortening.


Radiation Research | 2003

Long-Lived Mutagenic Radicals Induced in Mammalian Cells by Ionizing Radiation are Mainly Localized to Proteins

Jun Kumagai; Kiyonao Masui; Yoshiteru Itagaki; Masaru Shiotani; Seiji Kodama; Masami Watanabe; Tetsuo Miyazaki

Abstract Kumagai, J., Masui, K., Itagaki, Y., Shiotani, M., Kodama, S., Watanabe, M. and Miyazaki, T. Long-Lived Mutagenic Radicals Induced in Mammalian Cells by Ionizing Radiation are Mainly Localized to Proteins. Radiat. Res. 160, 95–102 (2003). We have provided evidence that long-lived radicals, produced by ionizing radiation, are highly mutagenic and transforming in mammalian cells. Long-lived radicals are scavenged effectively by vitamin C or by epigallocatechin-3-O-gallate (EGCG). Long-lived radicals are not involved in lethality or in the induction of chromosome aberrations. We now report the results of experiments that define the relative amounts of long-lived radicals in DNA and proteins and identify the major protein radicals as sulfinyl radicals (R-CH2-S-O·). To make these assignments, yields of long-lived radicals in γ-irradiated salmon sperm DNA and albumin were compared by ESR. ESR spectra of long-lived radicals produced in irradiated Syrian hamster embryo (SHE) cells were analyzed precisely and compared with ESR parameters obtained by density functional theory calculations. Long-lived radicals yields of 99.8% were produced in proteins. We also identified a new type of long-lived radical as H-added phenylalanine radicals. While our evidence does not rule out the possibility of important biological consequences of the low-level long-lived radicals created by radiation, it implicates radicals in proteins as playing a key role in genetic effects of ionizing radiation. We suggest that these novel radicals, wherever they reside, need to be considered in explanations of biological sequela of radiation.


Journal of Radiation Research | 2004

Involvement of Reactive Oxygen Species (ROS) in the Induction of Genetic Instability by Radiation

Hideyuki Tominaga; Seiji Kodama; Naoki Matsuda; Keiji Suzuki; Masami Watanabe


Mutation Research | 2004

Evidence for induction of DNA double strand breaks in the bystander response to targeted soft X-rays in CHO cells

Genro Kashino; Kevin Prise; Giuseppe Schettino; M. Folkard; Borivoj Vojnovic; Barry D. Michael; Keiji Suzuki; Seiji Kodama; Masami Watanabe


Cancer Research | 2003

Delayed reactivation of p53 in the progeny of cells surviving ionizing radiation.

Keiji Suzuki; Satoshi Yokoyama; Satomi Waseda; Seiji Kodama; Masami Watanabe


Biochemical and Biophysical Research Communications | 2004

X-ray-induced telomeric instability in Atm-deficient mouse cells

Barkhaa Undarmaa; Seiji Kodama; Keiji Suzuki; Otsura Niwa; Masami Watanabe


Journal of Radiation Research | 2004

Delayed Induction of Telomere Instability in Normal Human Fibroblast Cells by Ionizing Radiation

Mitsuaki Ojima; Hiroki Hamano; Masatoshi Suzuki; Keiji Suzuki; Seiji Kodama; Masami Watanabe


Carcinogenesis | 2003

Gap junctional intercellular communication and cellular response to heat stress

Nobuyuki Hamada; Seiji Kodama; Keiji Suzuki; Masami Watanabe


Biochemical and Biophysical Research Communications | 2004

Involvement of telomere dysfunction in the induction of genomic instability by radiation in scid mouse cells

Ayumi Urushibara; Seiji Kodama; Keiji Suzuki; Mohamad Desa; Fumio Suzuki; Takeki Tsutsui; Masami Watanabe

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