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 Münster, 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.