China
Africa
Explore chapters and articles related to this topic
Chemical Causes of Cancer
Published in Peter G. Shields, Cancer Risk Assessment, 2005
Gary M. Williams, Alan M. Jeffrey
One component of secondary prevention is the use of anticancer or che-mopreventive agents whose mechanisms were discussed earlier. A wide variety of experimental cancer preventive agents, both naturally occurring and synthetic, is known (177,391,454,455). Several of these have shown promise in humans (456), mostly as inhibitors of the growth of neoplastic cells. Among agents of this type, retinoids have been evaluated for suppression of oral cancer but high relapse rates and serious side effects occur (457). The selective estrogen receptor modulator tamoxifen reduces breast cancer risk (223,458). Also, breast (459) and colon (460) cancer risks are reduced by regular use of nonsteriodal anti-inflammatory drugs. Of particular interest is specific COX-2 inhibitors such as celecoxib, whose anticancer activity may result from a variety of effects (461), including reduction of enzyme-derived prostaglandins, particularly PGE2. Another strategy, the enhancement of carcinogen detoxification, is being pursued with agents such as oltipraz (177).
Vitexin protects melanocytes from oxidative stress via activating MAPK-Nrf2/ARE pathway
Published in Immunopharmacology and Immunotoxicology, 2020
Xiao-Sha Li, Xue-Yong Tang, Wei Su, Xin Li
The human skin system does have intrinsic antioxidant signaling pathways, and nuclear factor E2-related factor 2 (Nrf2) is one essential transcription factor responsible for protecting cells from oxidative damage [10]. Nrf2 has leucine zipper domains to bind to antioxidant response elements (ARE) and initiate the expression of downstream antioxidant proteins [11]. Nrf2 is a redox-sensitive transcription factor, and many of its downstream genes such as heme oxygenase 1 (HO-1) are critical in fighting against oxidative stress induced by ROS [12]. HO-1 catalyzes the reaction in which heme is broken down into biliverdin (an antioxidant agent), carbon monoxide (an anti-inflammatory agent), and iron. In previous studies, HO-1 is shown to be a suppressor for a variety of pathologies, including sepsis, hypertension, acute lung injury, and kidney injury [10,13,14]. It has been reported that Nrf2/ARE axis can regulate anti-inflammatory gene expression and inhibit the progression of inflammation [15]. Since ROS accumulation can induce the activation of Nrf2/ARE axis as tissue cells are responding to oxidative stress, we speculate that Nrf2/ARE signaling may have significant roles in vitiligo as well. Nrf2 has been the focus of several drug development efforts, but limits progress obtained so far with few projects focus on the field of vitiligo. Oltipraz is a clinical Nrf2 inducer that shows preclinical activities in terms of an anticancer agent [16]. However, clinical trials found significant side effects and minimal efficacy of oltipraz, while the compound itself may even generate ROS. Dimethyl fumarate, an approved drug for multiple sclerosis, is shown to have Nrf2 activation effect in vitro [17]. However, few research efforts are made in terms of applying dimethyl fumarate to vitiligo treatment.