Role of Vitamin C in Selected Malignant Neoplasms in Women

Abstract

Since the first reports describing the anti-cancer properties of vitamin C published several decades ago, its actual effectiveness in fighting cancer has been under investigation and widely discussed. Some scientific reports indicate that vitamin C in high concentrations can contribute to effective and selective destruction of cancer cells. Furthermore, preclinical and clinical studies have shown that relatively high doses of vitamin C administered intravenously in 'pharmacological concentrations' may not only be well-tolerated, but significantly improve patients' quality of life. This seems to be particularly important, especially for terminal cancer patients. However, the relatively high frequency of vitamin C use by cancer patients means that the potential clinical benefits may not be obvious. For this reason, in this review article, we focus on the articles published mainly in the last two decades, describing possible beneficial effects of vitamin C in preventing and treating selected malignant neoplasms in women, including breast, cervical, endometrial, and ovarian cancer. According to the reviewed studies, vitamin C use may contribute to an improvement of the overall quality of life of patients, among others, by reducing chemotherapy-related side effects. Nevertheless, new clinical trials are needed to collect stronger evidence of the role of this nutrient in supportive cancer treatment.

Keywords: breast cancer; cervical cancer; endometrial cancer; l-ascorbic acid; ovarian cancer; vitamin C.

Figure 1

Structure of vitamin C (l-ascorbic acid, ascorbate), its sodium salt (sodium l-ascorbate), and oxidized form (l-dehydroascorbic acid) plus additional information on vitamin C [1].

Figure 2

Mechanisms involved in the anti-cancer activity of vitamin C. A number of cell processes are targeted by vitamin C, by stimulating (green arrow) or inhibiting (red arrow) different pathways. AIF, apoptosis-inducing factor; CDK2, cyclin-dependent kinase 2; CHK2, checkpoint kinase 2; CHOP, C/EBP homologous protein; COX-2, cyclooxygenase-2; H2AX, histone 2AX; HIF-1α, hypoxia-induced factor 1α; NF-κB, nuclear factor-κB; Nrf2, nuclear factor erythroid 2-related factor 2; PARP, poly(ADP-ribose) polymerase; PG, prostaglandins; ROS, reactive oxygen species; SYNPO2, synaptopodin 2; TET, ten-eleven translocation; TRAIL, tumor necrosis factor (TNF)-related apoptosis-inducing ligand; YAP1, yes-associated protein 1 [21,26,27,28,32,38,68,69,70].

Figure 3

Antioxidant properties of vitamin C and redox cycling antioxidants. APX, ascorbate peroxidase; DHAR, semidehydroascorbate reductase; GPX, glutathione peroxidase; GR, glutathione reductase [86].