Reviewed studies indicated the effect of vitamin C on various lung disorders including asthma, COPD, lung fibrosis, lung cancer, lung infections as well as allergic and immunologic disorders with anti-inflammatory, antioxidant and immunomodulatory mechanisms, in both experimental and clinical studies.
Various experimental studies showed the relaxant effect of vitamin C on TSM mediated by various mechanisms including β2-adrenoceptors stimulatory, inhibitory effect on muscarinic and histamine H1 receptors, phosphodiesterase enzyme-like and calcium channel blocking mechanisms. These findings suggest the possible bronchodilatory effects of the vitamin C in obstructive respiratory diseases but further clinical trials should be performed to examine this effect in different obstructive pulmonary disorders.
The preventive effect of vitamin C was demonstrated in different respiratory diseases, including asthma, COPD, lung fibrosis, lung cancer, and other respiratory disorders.
Treatment with the vitamin C affects different lung cancer in vitro, in vivo and in clinical studies through affecting cell viability and other molecular mechanisms.
In experimental studies, the effects of vitamin C on lung infections caused by various viruses and batteries were reported. Clinical studies also demonstrate that timely administration of high dose of vitamin C improves the outcome of COVID-19 infection.
The preventive or prophylactic effects of the vitamin C on various allergic and immunologic disorders were also indicated. The possible cellular and molecular mechanisms of the preventive effects of vitamin C on various respiratory disorders were shown to be due to its anti-inflammatory, immunomodulatory and antioxidant properties in different studies. Anti-inflammatory effects of the vitamin C on lung inflammation were reported by reduction of total and WBC in BALF and blood of asthma and COPD and others respiratory disorders. Vitamin C also improved the levels of inflammatory mediators such as 8-isoprostanese, vascular endothelial growth factor, pro-inflammatory protein expressions such as Rtp801, NF-κB, and iNOS as well as MMP-9 and MMP-12 gene expression in the BALF and lung tissues. Regarding the antioxidant effects of vitamin C, it declined free radicals. Serum and BALF level of oxidants markers such as MDA and erythropoietin were reduced but antioxidants including catalase and glutathione peroxidase were increased in asthmatic animals by treatment with vitamin C. In addition, vitamin C suppressed ROS generation in cells and improved mitochondrial function as well as inflammation status. Immune-modulatory effects of vitamin C were indicated in animal models by decreasing serum and BALF levels of IL-6, IL-1β, TNFα, IL-4 and IL-5 but enhanced IFN-γ and Treg cells. Treatment with vitamin C also shifted Th1/Th2 balance toward the Th1 pole. In addition, vitamin C down-regulated gene expression of pro-inflammatory cytokines such as TNFα and IL-1 that is dependent on ROS by inhibiting NF-kB transcription. The levels of IL-4 and IL-5 in the BALF, IgE and IgG1 levels in the serum and NF-κB p65 protein levels in the lung tissue were improved by treatment with vitamin C. Lung pathological changes in various respiratory diseases and tracheal responsiveness to different stimuli, mainly methacholine, were improved due to vitamin C therapy which are suggested to be due to anti-inflammatory, antioxidant and immunomodulatory properties of this agent.
