Vitamin D Protects Pancreatic Cancer (PC) Cells from Death and DNA Damage Induced by Oxidative Stress.

In addition to its well-recognized roles in immunomodulation and calcium phosphate homeostasis, growing evidence shows that Vitamin D (Vit. D) presents a wide range of other properties, including antioxidant and anticancer effects. However, the action of Vit. D is not fully recognized in pancreatic cancer (PC) cells exposed to oxidative stress. Therefore, the aim of the present study was to investigate whether vitamin D (Vit. D) protects PC cells from death induced by oxidative stress. PC cells are suggested to be resistant to oxidative stress since they demonstrate overexpression of superoxide dismutase (SOD) 1-3. The study measured PC cell viability, DNA damage level, the mRNA and protein expression of antioxidant enzymes, reactive oxygen species (ROS) level and activity of antioxidant enzymes after exposure to HO, Vit. D and their combinations. N-Acetyl-L-Cysteine (NAC), a well-known direct ROS scavenger, was used as a positive control. Vit. D exposure alone had no effect on PC cell viability, ROS level and DNA damage. Its impact on the mRNA and protein expression of antioxidant enzymes was also scarce. However, Vit. D protected PC cells against HO-induced death, similarly to NAC. It also diminished the increase in ROS and DNA damage caused by HO. In addition, Vit. D enhanced the mRNA expression of catalase (CAT), SOD 1-3 and glutathione peroxidase (Gpx)3, but did not affect their protein levels in PC cells exposed to oxidative stress. Interestingly, Vit. D increased CAT activity after 24 h in 1.2B4 cells and elevated the activity of both CAT and Gpx after 2 h in PANC-1 cells, which could contribute to the observed reduction of HO-induced ROS level. To conclude, our findings show that antioxidant properties of Vit. D may protect PC cells from oxidative stress-induced death. Therefore, further studies are needed to understand the action of Vit. D in PC cells.