Vitamin D and its therapeutic relevance in pulmonary diseases.

Vitamin D is customarily involved in maintaining bone and calcium homeostasis. However, contemporary studies have identified the implication of vitamin D in several cellular processes including cellular proliferation, differentiation, wound healing, repair and regulatory systems inclusive of host defence, immunity, and inflammation. Multiple studies have indicated corelations between low serum levels of vitamin D, perturbed pulmonary functions and enhanced incidences of inflammatory diseases. Almost all of the pulmonary diseases including acute lung injury, cystic fibrosis, asthma, COPD, Pneumonia and Tuberculosis, all are inflammatory in nature. Studies have displayed strong inter-relations with vitamin D deficiency and progression of lung disorders; however, the underlying mechanism is still unknown. Vitamin D has emerged to possess inhibiting effects on pulmonary inflammation while exaggerating innate immune defenses by strongly influencing functions of inflammatory cells including dendritic cells, monocyte/macrophages, T cells, and B cells along with structural epithelial cells. This review dissects the effects of vitamin D on the inflammatory cells and their therapeutic relevance in pulmonary diseases. Although, the data obtained is very limited and needs further corroboration but presents an exciting area of further research. This is because of its ease of supplementation and development of personalized medicine which could lead us to an effective adjunct and cost-effective method of therapeutic modality for highly fatal pulmonary diseases.

Prophylactic action of linseed (Linum usitatissimum) oil against cyclophosphamide-induced oxidative stress in mouse brain.

The present study is a pilot study that explores the antioxidative properties of linseed (Linum usitatissimum) oil in its prophylactic action against oxidative stress induced by a radiomimetic drug, cyclophosphamide. Oral administration of linseed oil (0.1 mL/kg of body weight/day) for 20 days prior to an acute dose of cyclophosphamide (75 mg/kg) significantly inhibited the augmented level of malondialdehyde, conjugated dienes, and hydroperoxides in the mouse brain. The cyclophosphamide- induced decline in the levels of reduced glutathione, glutathione peroxidase, and alkaline phosphatase was also significantly prevented by linseed oil in mouse blood. Similarly, the increased activity of acid phosphatase and oxidized glutathione was significantly inhibited by linseed oil. Results clearly indicate the prophylactic action of linseed oil against cyclophosphamide- induced oxidative stress.