Antioxidant for younger arteries

C&I Issue 4, 2018

The ageing of blood vessels was turned back 15 to 20 years when older adults took commercially available antioxidant, scientists in the US report. The antioxidant targeted the biological batteries of cells – mitochondria – and the effects were seen within six weeks.

The researchers looked at how well the lining of blood vessels worked by measuring how people’s arteries expanded with increased blood flow. Poor flexibility in arteries is known to be a risk factor for coronary heart disease.

Artery blood flow was 42% higher after adults aged between 60 and 70 with impaired arteries took the antioxidant MitoQ. Plasma low-density lipoprotein – a marker of oxidative stress – was also lower in those receiving MitoQ than placebo (Hypertension, doi: 10.1021/acsbiomaterials.7b00959).

MitoQ is a modified form of the naturally occurring coenzyme ubiquinol, which is attached to a lipophilic, positively charged molecule. It can cross cell membranes and accumulate in mitochondria.

‘MitoQ can then reduce free radical production by the mitochondria and thereby decrease oxidative stress,’ explains first author Matthew Rossman at the University of Colorado. ‘Oxidative stress is a primary mechanism of vascular dysfunction, so decreasing oxidative stress has a positive effect on vascular function.’

The findings suggest that pharmaceutical-grade nutritional supplements, or neutraceuticals, could play a role in preventing heart disease.

The study is small, however, with 10 adults in the treatment group and 10 in the placebo group. Rossman says the results ‘provide a good starting point for future work in humans and suggest that therapies targeting the mitochondria may hold promise for improving vascular function with ageing.’

‘The issue of dietary antioxidants and coronary heart disease is a very controversial one,’ says David Leake, molecular scientist at the University of Reading, UK. ‘MitoQ is an antioxidant, but one with a difference in that it localises to the powerhouses of cells, the mitochondria, and inactivates toxic free radicals there.’

Leake notes that the improvement in artery dilation was not proven to be tied to a decrease in free radicals produced by mitochondria, although this seems likely based on other research findings.

‘The proof of the pudding will be if the drug decreases deaths from cardiovascular disease, but this would take a Phase 3 clinical trial of about five years with something like 10,000 cardiovascular disease patients,’ he says. ‘This would also indicate if there are any unexpected side effects of scavenging mitochondrial free radicals.’

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