BSc Zoology at the University of Bristol (1982) PhD (1988) in male reproductive toxicology

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

Brinkworth M.H., Weinbauer G.F., Schlatt S. and Nieschlag E. Identification of male germ cells undergoing apoptosis in male rats. Journal of Reproduction and Fertility 105: 25-33 (1995) Anderson D., Edwards A.J., Brinkworth M.H. and Hughes J.A. Male-mediated F1 effects in mice exposed to 1,3-butadiene. Toxicology 113: 120-127 (1996) Carani C., Gromoll J., Brinkworth M.H., Simoni M., Weinbauer G.F. and Nieschlag E. cynDAZ: a Cynomolgus monkey homologue of the human deleted-in-azoospermia (DAZ) gene. Molecular Human Reproduction 3: 479-483 (1997) Brinkworth M.H., Weinbauer G.F., Bergmann M. and Nieschlag E. Apoptosis as the mechanism of germ cell loss in elderly men. International Journal of Andrology 20: 222-228 (1997) Brinkworth M.H., Anderson D. Hughes J.A., Jackson L.I., Yu T.-W. and Nieschlag E. Genetic effects of 1,3-butadiene in mice. Mutation Research: special issue 397: 67-75 (1998) Edwards A.J., Anderson D., Brinkworth M.H. and Parry J.M. An investigation of male-mediated F1 effects in mice treated acutely and sub-chronically with urethane. Teratogenesis, Carcinogenesis, Mutagenesis: special issue 19: 87-103 (1999) Anderson D., Jenkinson P.C., Edwards A.J., Hughes J.A. and Brinkworth M.H. Paternal Legacies. (Commentary) Teratogenesis, Carcinogenesis, Mutagenesis: special issue 19: 105-108 (1999) Armour J.A.L., Brinkworth M.H. and Kamischke A. Direct analysis by small-pool PCR of MS205 minisatellite mutation rates in sperm after mutagenic therapies. Mutation Research 445: 73-80 (1999) Brinkworth M.H. and Nieschlag E. Cyclophosphamide-induced foetal abnormalities are associated with reduced paternal germ-cell apoptosis. Mutation Research. 447: 149-154 (2000) Brinkworth M. H. Paternal transmission of genetic damage: findings in animals and humans. International Journal of Andrology 23: 123-135 (2000) Weinbauer G.F., Aslam H., Krishnamurthy H., Brinkworth M.H., Einspanier A., and Hodges J.K. Quantitative analysis of spermatogenesis and apoptosis in the common marmoset (Callithrix jacchus) reveals high spermatogonial turnover and spermatogenic efficiency. Biology of Reproduction. In press Brinkworth M.H. and Handelsman D.J. Environmental influences on male reproductive health. Chapter 13 in "Andrology: Principles and Practice of Male Reproductive Health." 2nd edition. Eds, E.Nieschlag and H.M.Behre. Pub., Springer-Verlag Berlin Heidelberg. pp. 253-270 (2000)