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Male-mediated developmental toxicity

Asian Journal of Andrology 2014年第1期16卷 81-88页

作者： Diana Andersonl Thomas E Schmid adolf baumgartner Division of Medical Sciences School of Life Sciences University of Bradford Bradford West Yorkshire BD UK Department of Radiation Oncology Klinikum rechts der Isar Technische Universit~t MOnchen Munich Germany.

Male-mediated developmental toxicity has been of concern for many years. The public became aware of male-mediated developmental toxicity in the early 1990s when it was reported that men working at Sellafield might be causing leukemia in their children. Human and animal studies have contributed to our current understanding of male-mediated effects. Animal studies in the 1980s and 1990s suggested that genetic damage after radiation and chemical exposure might be transmitted to offspring. With the increasing understanding that there is histone retention and modification, protamine incorporation into the chromatin and DNA methylation in mature sperm and that spermatozoal RNA transcripts can play important roles in the epigenetic state of sperm, heritable studies began to be viewed differently. Recent reports using molecular approaches have demonstrated that DNA damage can be transmitted to babies from smoking fathers, and expanded simple tandem repeats minisatellite mutations were found in the germline of fathers who were exposed to radiation from the Chernobyl nuclear power plant disaster. In epidemiological studies, it is possible to clarify whether damage is transmitted to the sons after exposure of the fathers. Paternally transmitted damage to the offspring is now recognized as a complex issue with genetic as well as epigenetic components.

关键词： genetic and epigenetic effects human exposure to chemicals and radiation male-mediated animal studies paternalexposure to chemicals and radiation

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<i>In Vitro</i>Investigation of DNA Damage Induced by the DNA Cross-Linking Agents Oxaliplatin and Satraplatin in Lymphocytes of Colorectal Cancer Patients

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Journal of Cancer Therapy 2012年第1期3卷 78-89页

作者： Amal Alotaibi adolf baumgartner Mojgan Najafzadeh Eduardo Cemeli Diana Anderson Division of Biomedical Sciences University of Bradford Bradford UK.

Exposure to toxic chemicals, especially chemotherapeutic drugs, may induce several DNA lesions, including DNA interstrand crosslinks. These crosslinks are considered toxic lesions to the dividing cells since they can induce mutations, chromosomal rearrangements, and cell death. Many DNA interstrand crosslinks lesions can be generated by platinum-based chemotherapeutic agents. Satraplatin is a novel orally administered platinum-based chemotherapeutic agent. In the present study, we investigated DNA interstrand crosslinks lesions induced by oxaliplatin and satraplatin in lymphocytes obtained from colorectal cancer patients and healthy volunteers. Satraplatin demonstrated an increase in interstrand crosslinks in a dose-dependent manner in the Comet assay (p in vitro. Here, to the best of our knowledge we report for the first time evidence of DNA double strand breaks formation as a possible molecular mechanism of action for satraplatin.

关键词： DNA Interstrand Crosslinks Oxaliplatin Satraplatin γH2AX Foci Formation

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