For reasons as yet unexplainable, women with red hair appear to be more stoic when faced with pain, compared to women with other hair colour, and to men.
These findings, although preliminary, will be investigated in a study to be launched in Britain by the medical research council's Human Genetics Unit in Edinburgh.
Already a panel of redheads has been recruited to take part in the research.
Professor Ian Jackson, says one of the aims is to see if there is a natural mechanism at work in redheads that can be adapted to help develop new pain-killers and anesthetic.
According to Professor Jackson, people are interested in developing new anaesthetics or co-anaesthetics, as treatment for chronic pain is difficult.
In studies on "redhead" mice, which have blonde fur but carry a similar gene to the one that causes red hair in humans, scientists were able to target the pain-reducing mechanism.
Jackson says red-haired mice show a similar ability as human female redheads, to withstand higher pain thresholds compared to other mice and require less anaesthetic to block out certain pains.
The original work on red hair and pain was carried out by Professor Jeffrey Mogil, at McGill University in Montreal, Canada.
He identified a mutant version of a gene called melanocortin-1 (Mc1r), which is linked to ginger hair and fair skin.
This apparently gives women a higher pain threshold, but does not appear to have the same effect on men.
This is possibly explained by subtle differences in the way male and female brains process pain.
It appears that in most people, the Mc1r gene produces a protein that reduces the ability of opioid drugs to block pain.
However in redheaded women, who have a non-functional version of the gene, such painkillers are free to work unhindered.
As a result of several additional experiments done in his lab and by other groups, Dr. Hayward suspected that the mutant proteins might be more vulnerable than the normal enzyme to specific stresses in tissues. In their Journal of Biological Chemistry paper, Dr. Hayward and his colleagues at the University of Massachusetts Medical School show that when the mutant SOD1 enzymes are exposed to reagents that can disrupt some of the protein's bonds or remove its metal ions, they become much stickier than the normal protein.
"The mutants, but not the normal SOD1, adhere to a hydrophobic or 'greasy' surface, and this property could promote abnormal interactions with other proteins or membranes in the cell," explains Dr. Hayward. "How well different tissues can handle this burden of sticky protein, especially during aging, may be one factor that determines which cell types are most vulnerable in the disease. It was interesting to us that the adherent forms were not restricted to the nervous system in the mouse models but were also seen in other tissues such as heart and skeletal muscle. It is possible that this property could contribute to abnormalities in muscle, while other tissues such as kidney do not accumulate hydrophobic SOD1 despite a high expression level of the mutants."
These results may lead to new treatments for some forms of ALS. For example, if researchers can minimize the hydrophobic exposure or can understand how certain tissues prevent build-up of the sticky forms of SOD1, they might be able to boost defenses in tissues known to be susceptible to mutant SOD1 accumulation.
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