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

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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

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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.