Using Antioxidants Promotes ROS (free Radicals)

[ecstatichamster]

Antioxidant treatment induces reductive stress associated with mitochondrial dysfunction in adipocytes

β-Adrenergic stimulation of adipose tissue increases mitochondrial density and activity (browning) that are associated with improved whole-body metabolism. Whereas chronically elevated levels of reactive oxygen species (ROS) in adipose tissue contribute to insulin resistance, transient ROS elevation stimulates physiological processes such as adipogenesis. Here, using a combination of biochemical and cell and molecular biology–based approaches, we studied whether ROS or antioxidant treatment affects β3-adrenergic receptor (β3-AR) stimulation–induced adipose tissue browning. We found that β3-AR stimulation increases ROS levels in cultured adipocytes, but, unexpectedly, pretreatment with different antioxidants (N-acetylcysteine, vitamin E, or glutathione ethyl ester) did not prevent this ROS increase. Using fluorescent probes, we discovered that the antioxidant treatments instead enhanced β3-AR stimulation–induced mitochondrial ROS production. This pro-oxidant effect of antioxidants was, even in absence of β3-AR stimulation, associated with decreased oxygen consumption and increased lactate production in adipocytes. We observed similar antioxidant effects in wildtype mice:N-acetylcysteine blunted β3-AR stimulation–induced browning of white adipose tissue and reduced mitochondrial activity in brown adipose tissue even in the absence of β3-AR stimulation. Furthermore, N-acetylcysteine increased the levels of peroxiredoxin 3 and superoxide dismutase 2 in adipose tissue, indicating increased mitochondrial oxidative stress. We interpret this negative impact of antioxidants on oxygen consumption in vitro and adipose tissue browning in vivo as essential adaptations that prevent a further increase in mitochondrial ROS production. In summary, these results suggest that chronic antioxidant supplementation can produce a paradoxical increase in oxidative stress associated with mitochondrial dysfunction in adipocytes.

 

[ecstatichamster]

Special mention of cysteine in the form of NAC — increasing mitochondrial oxidative stress. Dr. Peat has said that cysteine, along with methionine and tryptophan, should be minimized in the diet if possible.

 

[moa]

I think the role of so called antioxidants is, when consumed with fruits, to lower bacterial activity in the small intestine related to sugar, or if some activity remains direct it to less harmful metabolites.

It may not have any good outcome if consumed without sugar, like in vegetables, as it may not have any function outside the digestive tract.

 

[Daniil]

Does this mean that vitamin E is harmful in a certain sense?

 

[Highserotonin90]

@Daniil An anti OX can act as a pro OX based on your Redox balance...so the response will always be subjective also based on the method of administration and dose used.