Limitation of oxidative damage

Ketone bodies cause oxidative damage. For example, cell membranes are damaged by lipid peroxidation and proteins are reduced by the oxidation of functional groups and subsequently limited in their function. In humans, oxidative damage is well known as cause of the comorbidities of diabetes mellitus 69.

Oxidative damage is triggered by

  • Direct prooxidant effects of acetone and acetoacetate 70, 71. The body tries to repel these prooxidative effects by converting them into β-hydroxybutyrate, but succeeds only to a limited extent in cases of severe glucose deficit.
  • Indirect prooxidative effect by activation of NADPH oxidases, MAP kinases and NF-κB 69. At the same time, ketone bodies have a pro-inflammatory effect.
  • These indirect prooxidative and proinflammatory effects are exacerbated by high concentrations of NEFA 72, 73.

Accordingly, oxidative damage from ketone bodies is especially to be expected in cases of

  • extreme glucose deficit
  • high NEFA concentrations
  • concomitant existence of inflammatory processes (mastitis, metritis, etc.)

Therefore, sufficient supplementation with antioxidants (vitamin E, β-carotine and selenium) is an important measure for the prevention and treatment of ketosis 21.

  • Acetoacetic acid

    •  good energy carrier

    •  moderately biocompatible

    •  oxidative damage


    •  Develops via spontaneous decarboxylation of acetoacetic acid

    •  oxidative damage

    ß-hydroxybutyrate (BHB)

    •  good biocompatibility: no redox damage

* see also our references page

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