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Quest for a male pill gets a wriggle on

Date

John Elder

Illustration: Matt Golding.

Illustration: Matt Golding.

AUSTRALIAN researchers have found a way to stop sperm swimming, opening another avenue for developing a male contraceptive pill and shedding light on possible causes of infertility in men.

The scientists were able to cut off the fuel supply to the ''motor'' that drives human sperm, so they are left twitching and not swimming.

Professor Moira O'Bryan, of Monash University's School of Biomedical Sciences, led the research with scientists from the University of Newcastle, John Curtin School of Medical Research and Garvan Institute of Medical Research, and the University of Cambridge, in Britain. Their study has been published in the journal PLoS Genetics.

In laboratory tests using mice, the team engineered a mutation in a gene called RABL2, which delivers protein fuel to the engine in a sperm's tail, known as the axoneme.

The mutation resulted in sperm tails that were 17 per cent shorter than normal, with a 50 per cent reduction in sperm production. The most striking result was that all mice with the mutated gene were rendered infertile, and their sperm unable to swim.

''They weren't wriggling or going anywhere, they were just twitching,'' says Professor O'Bryan. ''With this mutation, we get motors that don't work properly. To be fertile, sperm need motility … or swimming ability.''

Professor O'Bryan says a future male pill might work to inhibit the RABL2 gene rather than change it permanently. ''The challenge with developing the male pill isn't rendering the sperm infertile, but turning them back on again.''

But as RABL2 is also found - albeit in lower concentrations - in other tissues, such as the brain, kidney and liver, an inhibitor specific to the testes would be needed.

The fertility project was one part of an immense project involving experimental mutagenesis - the deliberate engineering of mutations on various genes - in laboratory mice.

Researchers looked at a variety of issues, including the immune system, hearing, facial abnormalities, diabetes and obesity.

Says Professor O'Bryan: ''It was like a big clinic where hundreds of mice were sorted into various projects. The ones that were fat were sent off in one direction, those with funny faces were sent elsewhere. A group in Sydney looked at lactation. Fertility was the last thing we tested.'' Mice with the genetic mutation were put in cages and observed for breeding behaviour. ''They all behaved normally,'' says Professor O'Bryan. ''But there were no pups born after six weeks. This was the result we were looking for. All of the males carrying this mutation were sterile.''

One in 20 men is infertile and, says Professor O'Bryan, the reasons for this are not understood.

''It's a bit of a mystery area. And people don't talk about it very often, they don't seek treatment.''

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