How Could Vitamin C Stop You From Developing Breast Cancer?

If you want to guard your wellbeing against excessive levels of oestrogen, which is a known risk factor of breast cancer, vitamin C can help you do it. This is according to researchers from the University of Missouri-Kansas City, who found that taking antioxidant supplements of vitamin C, or eating high amounts of vegetables that are rich in the vitamin, can help you to offset this nasty side effect of oestrogen.

Led by Bhupendra Singh and Hari K Bhat, the researchers discovered that vitamin C, which occurs naturally in green vegetables, and butylated hydroxyanisole (BHT), an artifical antioxidant commonly used in processed foods, can induce your body to produce superoxide dismutase 3. This helps to reduce a biomarker in your body that is associated with breast cancer, among other wellness concerns.

Excess levels of oestrogen can occur in your body because the female hormone is commonly used in contraceptives, as well as in hormone replacement therapy. According to experts, hormone replacement therapy and radiation used in diagnostics and cancer screening and treatment are the two biggest causes of breast cancer. Oestrogen plays in a role in the development of breast cancer because it induces DNA-damaging oxidative stress.

For the study, the researchers exposed female rats to, oestrogen, vitamin C, vitamin C plus oestrogen, BHT, and BHT plus oestrogen for up to eight months, finding that the antioxidant enzyme superoxide dismutase 3 was suppressed in the mammary tissues and tumours of the group of rats who were only exposed to oestrogen. However, in the rats that were also treated with vitamin C or BHT, the levels of superoxide dismutase 3 was less suppressed and there was less oxidative DNA damage. This indicates that antioxidants can overcome this suppression, and reduce breast cancer risk.

According to the researchers, ‘Increased DNA damage, colony and mammosphere formation, and migration in SOD3, knocked down MCF-10A cells, and nuclear translocation of SOD3 in vitamin C-treated mammary tissues and in MCF-10A cells suggest a protective role of SOD3 against DNA damage and mammary carcinogenesis.’ They concluded by saying, ‘Our studies further demonstrate that SOD3, but not SOD2 and SOD1, is induced by antioxidants and is regulated through NRF2. SOD3 may thus be an important gene in defence against oxidative stress and in the prevention of oestrogen-mediated breast cancer.’

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