Инфекция и иммунитет (Jan 2018)
PROTECTIVE ACTIVITY OF ASCORBIC ACID AT INFLUENZA INFECTION
Abstract
Abstract. Ascorbic acid (vitamin C, AA) is an essential nutrient of the human diet due to its participation on numerous regulatory and enzymatic processes. AA takes part in such vital physiological processes as hormone production, collagen synthesis, stimulation of the immune system, etc. In the present review the activities of AA are considered that provide its protective effect at influenza infection. This effect can be result of direct virus-inhibiting activity of AA as well as of anti-inflammatory and antioxidant properties. Oxidative stress during influenza infection leads to nonspecific damage of the pulmonary tissue and subsequent inflammation of the lungs. The antioxidant activity of AA results in alleviation of infection due to suppression of tissue damage as well as in inhibition of reactive oxygen species-mediated signal transduction and regulatory reactions. After oxidation by ROS, AA is converted to dehydroascorbic acid (DAA) and inhibits the key enzymes of NF-κB pathway, such as kinases IKKα and IKKβ. AA itself blocks the activity of another component of the NF-kB pathway, kinase IKKβ(SS/EE), whose activity is directed to the phosphorylation of the factor IκBα. As a result, activation of NF-κB and its transport to the nucleus does not occur. Thus, AA performs a dual function: first, it neutralizes free radicals, preventing them from activating NF-κB, and secondly, the product of its oxidation, DAA, further blocks the activation of this pathway. In addition, in some cases AA results in the decrease in the infectious activity of influenza virus that is not due to the antioxidant activity of AA, but to direct virus-inhibiting activity. Taken together, the presented data suggests that the use of drugs with antiviral and antioxidant activity, as a combination of individual drugs or, as in the case of AA, as a single drug with complex activity, for treatment of influenza has advantages over the etiotropic drug monotherapy scheme.
Keywords