1.
Association between vitamin C Intake and the risk of cervical neoplasia: A meta-analysis.
Cao, D, Shen, K, Li, Z, Xu, Y, Wu, D
Nutrition and cancer. 2016;(1):48-57
Abstract
To assess the association between vitamin C intake and cervical neoplasia (CN) risk. Databases including PubMed, Embase, and Springer link were retrieved up to June 10, 2014 with predefined strategy. The combined odds ratios (ORs) and their 95% confidence intervals (CIs) were calculated for overall and subgroup analyses. The publication bias was assessed using Begg's test and Egger's test. Sensitivity analysis was also conducted. Twelve studies consisting of 1 prospective cohort study and 11 case-control studies were included. In overall analysis, vitamin C intake was significantly associated with the reduced risk of CN (OR = 0.58; 95% CI: 0.44 to 0.75; P < 0.001). Subgroup analysis stratified by vitamin C dose indicated all dose categories achieved a reduced CN risk. Furthermore, increased vitamin C intake by 50 mg/day was related to the reduced risk of CN (OR = 0.92; 95% CI: 0.89 to 0.94; P < 0.05). No publication bias was detected by Begg's test (P = 0.169) and no apparent fluctuation was observed in summary OR by sensitivity analysis. Vitamin C intake was inversely associated with the risk of CN and this association was dose-dependent. However, more randomized controlled trials are required for further validation.
2.
Protective efficacy of vitamins C and E on p,p'-DDT-induced cytotoxicity via the ROS-mediated mitochondrial pathway and NF-κB/FasL pathway.
Jin, X, Song, L, Liu, X, Chen, M, Li, Z, Cheng, L, Ren, H
PloS one. 2014;(12):e113257
Abstract
Dichlorodiphenoxytrichloroethane (DDT) is a known persistent organic pollutant and liver damage toxicant. However, there has been little emphasis on the mechanism underlying liver damage toxicity of DDT and the relevant effective inhibitors. Hence, the present study was conducted to explore the protective effects of vitamin C (VC) and vitamin E (VE) on the cytotoxicity of DDT in HL-7702 cells and elaborate the specific molecular mechanisms. The results demonstrated that p,p'-DDT exposure at over 10 µM depleted cell viability of HL-7702 cells and led to cell apoptotic. p,p'-DDT treatment elevated the level of reactive oxygen species (ROS) generation, induced mitochondrial membrane potential, and released cytochrome c into the cytosol, with subsequent elevations of Bax and p53, along with suppression of Bcl-2. In addition, the activations of caspase-3 and -8 were triggered. Furthermore, p,p'-DDT promoted the expressions of NF-κB and FasL. When the cells were exposed to the NF-κB inhibitor (PDTC), the up-regulated expression of FasL was attenuated. Strikingly, these alterations caused by DDT treatment were prevented or reversed by the addition of VC or VE, and the protective effects of co-treatment with VC and VE were higher than the single supplement with p,p'-DDT. Taken together, these findings provide novel experimental evidences supporting that VC or/and VE could reduce p,p'-DDT-induced cytotoxicity of HL-7702 cells via the ROS-mediated mitochondrial pathway and NF-κB/FasL pathway.