著者
Suminori Akiba
出版者
日本環境変異原学会
雑誌
Genes and Environment (ISSN:18807046)
巻号頁・発行日
vol.35, no.3, pp.80-87, 2013 (Released:2013-09-03)
参考文献数
52
被引用文献数
1 5

Whether chronic exposure has an cancer risk per dose different from that of acute exposure is a topic of debate. This paper discusses the effect of dose rate on the strength of relationship between cancer risk and external exposure to low-LET (Linear Energy Transfer) ionizing radiation (such as X-rays and gamma rays), by reviewing important epidemiological studies. The study of atomic-bomb survivors, who had acute exposure mainly to low-LET ionizing radiation, has shown that the excess relative risk per gray (ERR/Gy) of leukemia increases in a linear-quadratic manner with an increase of radiation dose. The estimate of ERR/Gy for medium-high dose ranges was shown to be approximately two-fold larger than that for a low-dose range in the atomic-bomb survivor study. The estimate of ERR/Gy associated with acute exposure appears to be larger than those obtained from the studies of low-dose-rate exposure. On the other hand, the risk of solid cancer (or all cancers excluding leukemia) showed a linear dose-response relationship. Regarding the risk modification by dose rates, lower dose-rate exposure to high LET radiation is suspected to be associated with a larger risk. In the case of low-LET exposure, however, the cancer incidence study of residents in high natural background radiation areas of Karunagappally Taluk in Kerala State, India suggests that the ERR per dose for solid cancer after chronic radiation exposure is significantly lower than that associated with acute exposure such as that experienced by atomic-bomb survivors.
著者
Yun-Shan Li Ming-Fen Song Hiroshi Kasai Kazuaki Kawai
出版者
日本環境変異原学会
雑誌
Genes and Environment (ISSN:18807046)
巻号頁・発行日
vol.35, no.3, pp.88-92, 2013 (Released:2013-09-03)
参考文献数
16
被引用文献数
1 10

Human epidemiological studies have revealed significant increases in the cancer incidence rates by exposure to 100 mSv or higher doses of ionizing radiation. However, the relationship between lower doses of ionizing radiation and cancer incidence is still unclear. In general, oxidative DNA damage is closely related to cancer generation. We studied the oxidative DNA damage elicited by low dose ionizing irradiation. The γ-ray irradiation of a deoxyguanosine solution caused a linear increase in the 8-hydroxydeoxyguanosine (8-OHdG) levels, in the range of 20-300 mGy. Thus, 8-OHdG seems to be a good marker of the oxidative DNA damage caused by ionizing radiation. In contrast, in the case of the whole body X-ray irradiation of mice, the 8-OHdG levels in liver DNA and urine increased from about 500 and 200 mGy, respectively. These results indicate that living organisms have a defense mechanism against the oxidative damage caused by ionizing radiation. Considering the 8-OHdG levels as an ionizing radiation effect marker for living organisms, a threshold level of irradiation seems to exist for oxidative damage and tumorigenesis. Furthermore, diet imbalances increased radiation damage. Lifestyle may affect the radiation hazard.
著者
Jun Takada
出版者
日本環境変異原学会
雑誌
Genes and Environment (ISSN:18807046)
巻号頁・発行日
vol.35, no.3, pp.69-72, 2013 (Released:2013-09-03)
参考文献数
10
被引用文献数
1

Radiation hygiene survey has been conducted in the East Japan earthquake area, about Fukushima Dai-Ichi nuclear power station disaster caused by tsunami on March 11, 2011. Our surveys revealed that a public annual dose was 10 mSv following the disaster and health hazards should not be concluded by the methods of in situ dose evaluation. This study has been focused on internal dosimetries of iodine-131 in thyroid and of cesium-134, 137 in whole body. Further, we continuously have been studying radiation hygiene on cattle livestock in Namie town located within 20 km zone around the Fukushima Daiichi nuclear power station, and found no problem for the recovery.
著者
Shizuyo Sutou
出版者
日本環境変異原学会
雑誌
Genes and Environment (ISSN:18807046)
巻号頁・発行日
pp.2014.017, (Released:2014-06-07)
参考文献数
22
被引用文献数
1 1 1

Bipedalism paved the way to delivery of immature babies and development of the brain after birth. This communication presents the argument that hairlessness allowed hominins to access fire through wildfires, which occurred frequently after a climate shift from a wet to a dry environment 2.5 million years ago (Ma). Initially, naked hominins approached fire for warming, but soon must have come across burnt animals in the aftermath of wildfires. They learned the taste of burnt meat, which must have been a driving force compelling them to become meat-eaters. Hominins must have learned gradually how to control fire and how to repel hairy animals that abhor fire. Because they could neither run fast nor have muscles sufficiently strong to compete with large carnivores' fangs and claws, they chose not to be hunters but robbers. When they found that a carnivore had killed a prey animal, they approached the hungry predator and repulsed it using fire and stones, then claiming the prey intact. This is the core of the human robber hypothesis. The timing of global cooling, the appearance of savannahs, the appearance of transitional humans, decline of large predators, the manufacture of stone tools, and the start of cooking largely coincide at 2.5 Ma. They also smoked out animals from their dens or caves, and robbed them of shelter and territory. Cooked meat is both tasty and easily digested, providing hominins with rich nutrients sufficient to enlarge the brain, while most large carnivores were forced to extinction. Consequently, the use of fire, facilitated by hairlessness, must have played important roles in protecting hominins from cold, in repelling predators, in robbing large carnivores of prey and dwellings, and in providing the brain with nutrients for strong growth into adolescence. Development of the eccrine glands is also discussed as a result of hairlessness.
著者
Shizuyo Sutou Takashi Egawa Hiroki Mori Hiroaki Aso
出版者
日本環境変異原学会
雑誌
Genes and Environment (ISSN:18807046)
巻号頁・発行日
vol.35, no.3, pp.73-79, 2013 (Released:2013-09-03)
参考文献数
6
被引用文献数
2

The March 11 earthquake and tsunami crippled the Fukushima Daiichi Nuclear Power Plant of Tokyo Electric Power Company. Consequently, wide areas were contaminated with radioactive substances. The evacuation zone was set as the area within a 20 km radius from the power plant. People who lived in that zone were forced to evacuate immediately. Fukushima Prefectural Disaster Headquarters (FPDH) and the Japanese Governmental Disaster Headquarters (JGDH) planned to let them return to their homes temporarily and asked for help from related organizations, one of which is the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan. The ministry asked all Japanese universities and colleges to take part in screening radioactivity of the temporal returnees from the areas, with aids of the temporal returning program. We applied to the screening activities and measured radioactivity of the returnees at Bajikoen Off-site Center on July 14-17, 2011, and at Kawauchi Gymnasium or Hirono Central Gymnasium Off-site Center on July 23-25, 2011, in Fukushima Prefecture. During these periods, 4009 returnees in all were screened at these three Off-site Centers. None was found to be contaminated with radioactivity over 13,000 cpm. Before the returnee screening program, emergency screening had been conducted soon after the disaster. In all, 33,598 people out of 78,000 evacuees (43%) were screened during March 12-December 7, 2011, during which 3,686 volunteers were recruited by MEXT for the screening program. This is a tiny fraction of the temporal returning program. FPDH reported that 102 people were contaminated with more than 100,000 cpm out of 259,108 people generally screened from March 13, 2011-October 10, 2012. The 102 were detected only in the screening in March in 2011. No hazardous effect, however, was detected among them, so far. Screening is still underway. The present article was compiled to record aspects of the large scale radioactivity monitoring program planned by FPDH and JGDH.
著者
Mayukh Banerjee Pritha Bhattacharjee Ashok K. Giri
出版者
The Japanese Environmental Mutagen and Genome Society
雑誌
Genes and Environment (ISSN:18807046)
巻号頁・発行日
vol.33, no.4, pp.128-140, 2011 (Released:2011-11-29)
参考文献数
200
被引用文献数
20 28

Chronic exposure to the toxic metalloid arsenic, either through occupational or environmental route results in the development of a plethora of dermatological as well as non-dermatological health effects, multi-organ cancers being the most severe ones. Several epidemiological studies have reported the occurrence of different types of cancers in populations exposed chronically to arsenic from different corners of the globe, but the spectrum of symptoms and severity vary widely. Several genetic and environmental factors might play an important causal role for such observed differences, including genetic polymorphisms, dietary habits and socio-economic status of the population. Unfortunately, the paradoxical nature of this carcinogen makes the use of animal model systems unsuitable, since they do not reflect the exact in vivo condition of arsenic exposure in human beings. Hence, in this present review, we have attempted to collate the isolated pieces of information available in existing literature depicting the various forms of arsenic-induced cancers, variations and etiology thereof. We have attempted to depict the entire spectrum of carcinogenic outcomes of chronic arsenic exposure and the interactions among several components like, genes (polymorphisms and mutations), environmental factors and dietary factors in the process. The literature reviews are primarily based on the human beings (in vivo), but to understand the underlying mechanism, we have also collated the information based on cell line models, and animal models where human data is scanty or unavailable. Thus, here we present a comprehensive review on the current state of research in the field of arsenic-induced cancer and explore the underlying mechanism of arsenic-induced carcinogenicity, along with relevant historical perspective.
著者
Yun-Shan Li Kazuaki Kawai Hiroshi Kasai
出版者
The Japanese Environmental Mutagen and Genome Society
雑誌
Genes and Environment (ISSN:18807046)
巻号頁・発行日
vol.29, no.3, pp.128-132, 2007 (Released:2007-09-12)
参考文献数
24
被引用文献数
7 6

To clarify the in vivo genotoxic potential of dietary style, the amounts of 8-hydroxydeoxyguanosine (8-OH-dG), a marker of oxidative DNA damage, were determined by a high-performance liquid chromatography system coupled to an electrochemical detector (HPLC-ECD) in the urine of female mice to which a vitamin-deficient diet (for two months) and a sweet beverage (for two weeks) were administered. The urinary 8-OH-dG levels were clearly increased in these studies. In the vitamin-deficient diet experiment, the urinary 8-OH-dG levels were increased to 1.2-fold and 1.4-fold after one month and two months, respectively. When mice were given a commercially available sweet beverage instead of water for two weeks, the urinary 8-OH-dG was increased to 1.4-fold. In the sweet beverage experiment, significant increases of the volume consumed per day were observed, as compared to the control group (water). Although the total caloric intake per day was not remarkably different between the sweet beverage- and control-group, the mice in the sweet beverage group obtained a higher ratio of calories from sugar components. These results indicated that the elevation of oxidative stress could be caused by the prolonged intake of an unbalanced diet, such as a vitamin-deficient diet or one including sweet beverages.
著者
Shinji Oikawa
出版者
The Japanese Environmental Mutagen Society
雑誌
Genes and Environment (ISSN:18807046)
巻号頁・発行日
vol.30, no.1, pp.1-9, 2008 (Released:2008-03-25)
参考文献数
61
被引用文献数
1 3

Modification of DNA is believed to be a key step in mutagenesis and carcinogenesis. Reactive oxygen species (ROS) generated by environmental factors can cause oxidative DNA damage. This review focused on the role of oxidative DNA damage in mutagenesis and carcinogenesis mediated by environmental factors. This research investigated the mechanism of DNA damage induced by environmental chemicals and dietary factors using 32P-labeled DNA fragments obtained from the c-Ha-RAS-1 protooncogene and the p16 and p53 tumor suppressor genes. In addition, the content of 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG) was measured by using a high performance liquid chromatograph equipped with an electrochemical detector. 8-oxodG is probably one of the most abundant DNA lesion formed during oxidative stress. Antioxidants are considered as the most promising chemopreventive agents against various human cancers. However, some antioxidants play paradoxical roles acting as “double-edged sword”. The present research also investigated the mechanism of DNA damage induced by antioxidants using human cultured cell lines and 32P-labeled DNA fragments. This review shows recent experimental results and discusses the mechanisms of oxidative DNA damage in relation to carcinogenesis.
著者
Keiko Inami Masataka Mochizuki
出版者
The Japanese Environmental Mutagen Society
雑誌
Genes and Environment (ISSN:18807046)
巻号頁・発行日
vol.30, no.3, pp.71-76, 2008 (Released:2008-09-09)
参考文献数
12
被引用文献数
2 2

2-Acetylaminofluorene (AAF) is a procarcinogen and its activation mechanisms have been investigated in detail. AAF was metabolized to 2-acetylamino-9-fluorenone (AAF=O) and 2-acetylamino-9-fluorenol by S9 mix. The mutagenicity of AAF=O in the presence of S9 mix was equal in potency to that of AAF in Salmonella typhimurium TA1538, but the activation mechanism of AAF=O was poorly reported. In this study, we investigated possible ultimate species derived from AAF=O; N-hydroxy-2-acetylamino-9-fluorenone (N-OH-AAF=O), N-acetoxy-2-acetylamino-9-fluorenone (N-OAc-AAF=O), N-hydroxy-2-amino-9-fluorenone (N-OH-AF=O), and N-acetoxy-2-trifluoroacetylamino-9-fluorenone (N-OAc-TFAAF=O), a model compound for N-acetoxy-2-amino-9-fluorenone (N-OAc-AF=O), were synthesized and their mutagenicity was examined in S. typhimurium TA1538. The activation mechanism in S. typhimurium TA1538 was also investigated. The compounds in order of decreasing mutagenicity are N-OAc-TFAAF=O>N-OH-AF=O>N-OAc-AAF=O> N-OH-AAF=O. AAF=O is at least partially responsible for the mutagenicity of AAF, since a small amount of AAF is oxidized to AAF=O in the presence of S9 mix. Furthermore we suggest that an ultimate active species of AAF=O in S. typhimurium is N-OAc-AF=O, with the same activation manner as AAF.
著者
Tohru Shibuya Yukiharu Horiya
出版者
日本環境変異原学会
雑誌
Genes and Environment (ISSN:18807046)
巻号頁・発行日
vol.33, no.2, pp.34-42, 2011 (Released:2011-05-25)
参考文献数
93
被引用文献数
4

Epigenetics (EG) is a highly regulated biochemical mechanism underlying the expression of genes related to development and cellular differentiation that is disrupted by environmental stressors including chemicals and radiation. Studies of these phenomena are known as environmental epigenetics (EEG). Regulation of gene expression by the epigenetic mechanism is deeply involved in the developmental stages of animals and humans. EEG is, therefore, very important in the field of toxicology because it deals with the state of gene expression in all types of somatic and germ cells disrupted by environmental chemicals. We propose here an “Embryo-originated Epigenetic Toxicology Method (EEGT)”. In this method embryonic somatic and germ cells are treated with test substances and various toxicological phenomena in whole bodies are examined. Observations on transgenerational effects are also important in this method. This new method could unite various toxicological phenomena based on EEG.
著者
Shizuyo Sutou
出版者
日本環境変異原学会
雑誌
Genes and Environment (ISSN:18807046)
巻号頁・発行日
pp.2014.019, (Released:2014-06-19)
参考文献数
81
被引用文献数
2

Three characteristics, i.e., bipedalism, nakedness, and the family reproductive unit, distinguish humans from other primates. Once a hairless mutation was initially introduced, these three could be explained inseparately. All primates except humans can carry their babies without using their hands. A hairless mother would be forced to stand and walk upright to hold a baby. As her activities were markedly limited, the male partner had to collect food and carry it to her to keep their baby from starving. He must have been sexually accepted by her at any time as a reward for food. Sexual relations irrespective of estrus cycles might have strengthened the pair bond, leading to family formation. Savannahs appeared 2.5 million years ago (Ma), which forced hominins to terrestrial life, but the ground was full of danger and a larger brain became advantageous. Wildfires occurred frequently; naked hominins approached fire for warming, but soon must find burnt animals in the aftermath of wildfires. The taste of burnt meat must be a driving force for hominins to become meat-eaters. They must have learned how to control fire and how to repel hairy animals that hate fire. To compete with large carnivores with fangs and claws, they became not hunters but robbers. When robber hominins found that a carnivore had killed a prey animal, they approached the predator and repelled it away from the victim using fire, then claiming the prey intact. Major events such as the timing of global cooling, the appearance of savannahs, the appearance of early humans, decline of large predators, the manufacture of stone tools, and the start of cooking largely coincide at 2.5 Ma. Cooked meat must be tasty and easily digested, providing hominins with nutrients sufficient to enlarge the brain, while most large carnivores were forced to extinction. Thus, hairlessness created humans.
著者
Tetsuji Nagao Naomi Takada Noriko Onoda
出版者
日本環境変異原学会
雑誌
Genes and Environment (ISSN:18807046)
巻号頁・発行日
vol.33, no.2, pp.50-60, 2011 (Released:2011-05-25)
参考文献数
82
被引用文献数
1 2

Congenital malformations can be induced in the offspring of laboratory animals treated with the mutagens, ethylnitrosourea, methylnitrosourea, mitomycin C, triethylenemelamine or procarbazine before copulation. The spectra of malformations in the offspring classified as male-mediated malformations after exposure of paternal mice to mutagens showed no evidence of mutagen-specificity or germ-cell stage-dependent variations. Recently, we demonstrated the increased incidence of congenital malformations in the offspring of male mice exposed in utero to synthetic estrogens such as diethylstilbestrol (DES), 17β-estradiol (E2) or ethynyl estradiol (EE), and that the induction of male-mediated malformations by DES, E2 or EE showed a clear threshold effect. Developmental exposure to DES, E2 or EE caused partial atrophy and feminization in the genital tract. They also showed transgenerational effects when applied prenatally at a dose which caused histopathological changes in the testes. Germ-cell series in normal testis have mechanisms to select against spontaneously arising mutation; but these selection mechanisms may not function efficiently in chemically-damaged testes. Based on these results and considerations, we propose as a hypothesis that transgenerational teratogenesis by prenatal exposure to synthetic estrogens may occur as a consequence of testicular toxicity. Moreover, since DES has been reported to be non-genotoxic, epigenetic mechanisms such as DNA methylation may be involved in the transgenerational teratogenesis induced by estrogenic drugs. The expression patterns of DNA methyltransferases (Dnmts) mRNA, global DNA methylation levels in testicular cells of embryos exposed to estrogenic drugs or in epididymal sperm of mature male mice exposed prenatally to estrogenic drugs were different from those in the controls. Results shown in this review support the proposal that, when evaluating the toxicities of environmental chemicals including endocrine disruptors, epigenetic effects such as DNA methylation should be taken into account.