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Treating Sperm With Missing Protein Might Help Male Fertility

FRIDAY, Sept. 21 (HealthDay News) -- Some forms of male infertility could possibly be treated with a missing protein, an early new study suggests.

Sperm transfers this vital protein -- known as known as PLC-zeta (PLCz) -- to an egg during fertilization to trigger the processes needed for embryo development.

In lab experiments, researchers were able to prepare active human PLCz. They found that adding PLCz to sperm with defective protein allowed for fertilization.

This, they say, could significantly increase the likelihood of a successful pregnancy.

"We know that some men are infertile because their sperm fail to activate eggs. Even though their sperm fuses with the egg, nothing happens. These sperm may lack a proper functioning version of PLCz, which is essential to trigger the next stage in becoming pregnant," study co-leader Tony Lai, a professor at Cardiff University's Institute of Molecular and Experimental Medicine, said in a university news release.

"However, when an unfertilized egg is injected with human PLCz, it responds exactly as it should do at fertilization, resulting in successful embryo development to the blastocyst stage, vital to pregnancy success," Lai said.

The researchers' methods were limited to laboratory experiments and could not be duplicated in a fertility clinic in the same way, Lai acknowledged. Still, he said, the findings might lead to the development of a new treatment for men with certain forms of infertility.

"In the future, we could produce the human PLCz protein and use it to stimulate egg activation in a completely natural way," he concluded. "For those couples going through IVF treatment, it could ultimately improve their chances of having a baby and treat male infertility."

The study was published online Sept. 21 in the journal Fertility and Sterility.

More information

Visit the U.S. National Institutes of Health to learn more about male infertility.

-- Mary Elizabeth Dallas

SOURCE: Cardiff University, news release, Sept. 21, 2012

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