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Titlebook: Liver and Environmental Xenobiotics; S. V. S. Rana,K. Taketa Book 1997 Springer-Verlag Berlin Heidelberg 1997 Stress.drug.liver.metabolism

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发表于 2025-3-21 20:05:08 | 显示全部楼层 |阅读模式
书目名称Liver and Environmental Xenobiotics
编辑S. V. S. Rana,K. Taketa
视频video
图书封面Titlebook: Liver and Environmental Xenobiotics;  S. V. S. Rana,K. Taketa Book 1997 Springer-Verlag Berlin Heidelberg 1997 Stress.drug.liver.metabolism
描述The general populations are incidentally exposed to a wide variety of xenobiotics as a consequence of the pollution of the environment by industrial and agricultural chemicals. Xenobiotics entering the animal will undergo one or more of the following fate: (a) elimination unchanged, (b) metabolism by enzymes, (c) spontaneous chemical transformation and (d) remain unchanged in the body. The actions of xenobiotics on the body exhibit certain specificity depending upon the compound‘s chemical structure and reactivity. Since the processes of metabolism change these chemical properties ofaxenobiotic, bewildering number of reactions continue to pose new challenges to toxicologists and pharmacologists. It necessitates periodic and precise revision of the subject. This book contains invited contributions from learned colleagues that offer an excellent survey of and profound insight into the disposition and metabolism of a few environmentally and industrially significant xenobiotics. The topics range from an assessment of drug metabolising enzymes in the liver, DNA damage by reactive oxygen species generated by pesticides, role of NO in liver injury, hepatotrophicgrowth factor in liver rege
出版日期Book 1997
关键词Stress; drug; liver; metabolism; oncogene; pesticide
版次1
doihttps://doi.org/10.1007/978-3-662-12385-0
isbn_softcover978-3-662-12387-4
isbn_ebook978-3-662-12385-0
copyrightSpringer-Verlag Berlin Heidelberg 1997
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Generation of Reactive Oxygen Species, DNA Damage and Lipid Peroxidation in Liver by Structurally Dre classified as pesticides or contaminants of pesticides, and/or environmental pollutants. PCH such as endrin and chlordane, and CAH such as alachlor are halogenated and lipophilic [1–3], while OPS as fenthion and chlorpyrifos are organic triesters of phosphoric acid and phosphorothioic acid and are also lipophilic and highly toxic [3].
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Liver Injury: Genetic factors in alcohol and acetaldehyde metabolism,The number of patients with alcoholic liver disease (ALD) has increased recently in parallel with the increase in alcohol consumption in Japan as it is throughout the world [1]. However, heavy drinkers do not always develop ALD, indicating that genetic factors may be involved.
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Experimental Hepatocarcinogenesis and Its Prevention,In Japan, hepatocellular carcinoma (HCC) is mainly caused by viruses such as HBV and HCV. Twenty cases per 100,000 population suffer from HCC.
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Undifferentiated Gene Expression as the Entity of Liver Injuries,In a series of studies analyzing enzyme activities of carbohydrate and related metabolism in injured livers as well as serum levels of .-fetoprotein (AFP) and its sugar chain in acute liver injury, undifferentiated phenotypes were noted as a common feature of hepatic injuries of different etiologies [1–8].
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