Abstract
A hypothesis is proposed to explain the increased detrimental effect of COVID-19 for Black, Asian and Minority Ethnic (BAME) men and women compared to Caucasian individuals. This is based on the differing photochemistry of phaeomelanin in fair skin and eumelanin in dark/black skin. It is suggested that a range of reactive oxygen species, including, singlet oxygen and the superoxide radical anion, derived via direct photolysis of phaeomelanin, may escape the melanocyte and cause subsequent damage to the SARS-CoV-2 virus. It is further suggested that (large) carbon and sulphur peroxy radicals, from oxygen addition to radicals formed by carbon–sulphur bond cleavage, may assist via damage to the cell membranes. It is also speculated that light absorption by phaeomelanin and the subsequent C-S bond cleavage, leads to release of pre-absorbed reactive oxygen species, such as singlet oxygen and free radicals, which may also contribute to an enhanced protective effect for fair-skinned people.
Highlights
It is well established, but not yet understood, that COVID-19 is more damaging, for Black, Asian and Minority Ethnic (BAME) men and women and, even allowing for social aspects there still appears to be an increased detrimental effect, with Black Africans having the highest death rates (by a factor of two compared with White (Caucasian) individuals) [1, 2]
Since no molecular mechanism is established for the increased risk of COVID-19 among BAME communities, it is worth considering possible photochemical processes in the skin, generating and releasing activated oxygen species, free radicals, metal ions
While there is strong support for the beneficial value of vitamin D [3,4,5], there are reports that do not support a potential link between vitamin D concentrations and risk of COVID-19 infection, nor that vitamin D concentration may explain ethnic differences in COVID-19 infection [6]
Summary
The role of SO is worthy of discussion even though it may be too short lived to be of relevance to this hypothesis. Once in the blood stream, the lifetime is much reduced (to 4.2 μs in H2O – a factor of 13 times compared to D 2O) [31] so it may well have significantly decayed (minimum 6% left) before it can contribute to our hypotheses of virus inactivation. While a possible role for SO seems unlikely it should not be totally dismissed since we saw zero deactivation of SO in D2O for migration into the lipid bilayer [24]. Another aspect is that EM quenches SO itself, but, there is reduced EM in fair skinned people so this route to deactivation of SO is less significant
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