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Dr Martin Brinkworth

Associate Professor

Faculty/Dept/School School of Chemistry and Bioscience
(Faculty of Life Sciences)
Telephone +441274 233584


My first degree was in Zoology at the University of Bristol (1982) from which I acquired keen interests in reproductive biology and evolution. I then studied for a PhD (1988) in male reproductive toxicology, while working at a toxicology research institute (BIBRA, Carshalton, 1982-1992) where I acquired experience in genetic and reproductive toxicology. During this time I also spent a year (1989) as a Scientific Research Fellow at the National Cancer Center Research Institute, Tokyo, where I learnt a large range of molecular biology techniques studying food mutagen-induced liver tumourigenesis. Most recently I spent nearly 7 years (1992-1999) at the Institute of Reproductive Medicine of the University of M√ľnster, Germany. This is a centre for basic and clinical research in andrology and my work there encompassed male germ-cell apoptosis (a process of cellular suicide) and male-mediated teratogenicity (the study of abnormalities in the F1 generation following paternal exposure to DNA-damaging agents). At the University of Bradford I took those interests forward to demonstrate that exposure of primordial germ cells to genotoxins produced multiple genotoxic and non-genotoxic effect on sperm produced when the animals matured. And, in other work, that men with idiopathic male infertility show a range of types of genetic damage in their sperm. I also worked on projects investigating the role of RNA in sperm and demonstrating that sperm histone packaging has biological significance, in collaboration with colleagues at the University of Leeds. Building on the major impact of the second of those projects, I have been studying whether the presence of sperm histones influences patterns of sperm DNA damage. I have also been developing and using a novel in vitro tests for male reproductive toxicity. Most recently, I and colleagues at Bradford discovered, using a combination of computational and molecular biological approaches, that a specific type of adhesion molecule that is not expressed in the normal, adult human testis, is expressed whenever spermatogenic damage is present. It appears to be a universal marker and the finding is likely to have major importance in infertility diagnostics, male infertility treatment, and male contraception.


My principal research interest can be summarised as the process and consequences of genetic damage in the male germ-line. Such damage can be induced by a variety of exposures, notably from therapeutic, occupational, recreational and environmental sources. This can have a variety of different effects on spermatogenic cells, including cell-cycle arrest, DNA repair, apoptosis or the fixation of mutations in the genome. These phenomena may affect the fertility or fecundity of the individual but can also result in the transmission of heritable mutation to the F1 generation. Conventionally, it is believed that spontaneously arising, mutations vertically transmitted in this way are the basis for evolutionary change, although the vast majority of observable mutations are deleterious. It is known that organisms are potentially exposed constantly to DNA-damaging agents both from endogenous and exogenous sources. However, it is not yet fully understood how or under what circumstances alterations occur in the germ-line or what might be their consequences.