Even a small increase in temperature during sperm production can amplify DNA damage, new research suggests.
It is well known that the optimal temperature for sperm production is slightly lower than normal body temperature, but the molecular mechanisms underpinning this are not completely understood. Researchers at the University of Oregon looked at how DNA damage in sperm is caused following exposure to heat using Caenorhabditis elegans (C. elegans), a type of roundworm as a biological model.
'In both humans and C. elegans, relatively small increases in temperature are sufficient to reduce male fertility,' said co-author Dr Diana Libuda from the Department of Biology.
Using C. elegans, the team were able to observe developing sperm and eggs under the microscope, both under heat-stressed and normal conditions, which would be impossible in human subjects. They then sequenced the genomes of the resulting gametes to assess changes in the DNA, specifically focusing on transposons.
Transposons are pieces of DNA that move around between different locations in the genome, but this movement is usually suppressed during meiosis, as it can lead to harmful mutations.
Their results, published in the journal Current Biology, showed elevated levels of DNA damage in sperm – but not eggs – produced under heat-stressed conditions. A temperature difference of two degrees Celsius resulted in a 25-fold increase in DNA damage compared to sperm produced at normal temperatures. When these damaged sperm were used to fertilise eggs they did not develop into offspring.
'We found that after heat shock, certain transposons are found in new and more variable locations in the male genome,' said lead author Dr Nicole Kurhanewicz. 'The data presented in this paper suggest that another way egg and sperm develop differently is in how tightly they control the ability of mobile DNA elements, which are also known as 'jumping genes' or transposons, to move in the genome, and how sensitive to heat stress those mechanisms are in preventing that movement.'
The study offers an avenue for researchers to see if the same mechanisms contribute to male infertility in humans.
'This is where it gets exciting,' said Professor Scott Hawley, a meiosis researcher at the Stowers Institute for Medical Research in Kansas City, Missouri, who was not involved in the research. 'If we can determine how much of a change is bad, and if you are really concerned about the environmental matters such as hot tubs or 'boxers versus briefs', this type molecular understanding may allow us to reframe the debate on solid scientific grounds.'
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