Vitamin C Protects Against Tumors In Rodent Model Of Breast Cancer

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July 7, 2009

Vitamin C protects against tumors in rodent model of breast cancer

Vitamin C protects against tumors in rodent model of breast cancer

In the July, 2009 issue of the journal Carcinogenesis, researchers at Columbia University report the discovery of a protective property for vitamin C against estrogen-induced breast tumors in an estrogen-dependent breast tumor-sensitive strain of rats.

In their introduction to the article, the authors remark that estrogens can stimulate cancer through estrogen receptor dependent and independent mechanisms. The estrogen receptor-independent pathway of estrogen-induced breast cancer involves the activation of the body's estrogens by cytochrome P450 enzymes to generate catechol estrogens that can have adverse effects on DNA when undergoing oxidative metabolism. The current study was designed to determine whether reducing the metabolism of estrogen to catechol estrogens with the estrogen metabolic inhibitor alpha-napthoflavone (ANF) and lowering oxidative stress with the antioxidant vitamin C would reduce the development of estrogen-induced tumors.

The researchers divided the animals to receive a control substance, the estrogen 17-beta-estradiol (E2), vitamin C (added to drinking water), alpha-napthoflavone, 17-beta-estradiol plus vitamin C, or 17-beta-estradiol plus alpha-napthoflavone. Each of these groups was divided to receive treatment for 7, 15, 120 or 240 days.

At the end of each treatment period, the animals were examined for tumor incidence, and mammary and liver tissue levels of the oxidative stress marker 8-iso-Prostane F-2-alpha and the antioxidants superoxide dismutase, catalase, and glutathione peroxidase.

While no mammary tumors were found in the groups that did not receive estradiol, 82 percent of the rats that received estradiol alone developed mammary tumors after 240 days. In animals that received estradiol and vitamin C for 240 days, mammary tumor incidence was reduced to 29 percent. Tumors appeared later in those that received vitamin C and were mostly encapsulated, as opposed to the invasive tumors found in the estradiol only group.

Treatment with alpha-napthoflavone completely prevented tumors in rats that received estradiol. Alpha-napthoflavone and vitamin C were also found to lower oxidative stress in estradiol-treated animals. While SOD and glutathione peroxidase increased in animals exposed to estradiol alone, they remained unchanged compared to controls in animals that received estradiol with ANF and vitamin C, which suggests that the increased oxidative stress experienced by the rats that received estradiol alone resulted in enhancement of these antioxidant enzymes.

"The present study is the first to demonstrate the inhibition of breast carcinogenesis by antioxidant vitamin C or the estrogen metabolic inhibitor ANF in an animal model of estrogen-induced carcinogenesis," the authors announced. "These results suggest that E2 metabolism and oxidant stress are critically involved in estrogen-induced breast carcinogenesis.

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Health Concern Life Extension Highlight

Breast cancer

Breast cancer occurs when cells in the breast tissue divide and grow without control. The cell cycle is the natural mechanism that regulates the growth and death of cells. When the normal cell regulators malfunction and cells do not die at the proper rate, there is a failure of cell death (apoptosis) therefore cell growth goes unchecked. As a result, cancer begins to develop as cells divide without control, accumulating into a mass of extra tissue called a tumor. A tumor can be either non-cancerous (benign) or cancerous (malignant). As a tumor grows, it elicits new blood vessel growth from the surrounding normal healthy tissues and diverts blood supply and nutrients away from this tissue to feed itself. This process is termed “angiogenesis”- the development (genesis) of new blood vessels (angio). Unregulated tumor angiogenesis facilitates the growth of cancer throughout the body.

Cancer cells have the ability to leave the original tumor site, travel to distant locations, and recolonize. This process is called metastasis and it occurs in organs such as the liver, lungs, and bones. Both the bloodstream and lymphatic system (the network connecting lymph nodes throughout the body) serve as ideal vehicles for the traveling cancer. Although, these traveling cancer cells do not always survive beyond the tumor, if they do survive, the cancer cells will again begin to divide abnormally and will create tumors in each new location. A person with untreated or treatment-resistant cancer may eventually die of the disease if vital organs such as the liver or lungs are invaded, overtaken, and destroyed.

Cancerous tumors in the breast usually grow slowly. It is thought that by the time a tumor is large enough to be felt as a lump, it may have been growing for as long as 10 years. This has lead to the belief that undetectable spread of tumor cells (micrometastasis) may have already occurred by the time of the diagnosis. Therefore, preventive measures such as a healthy balanced diet and lifestyle, nutritional supplementation, and exercise are of primary importance against the development of cancer. Early diagnosis is the best way to reduce the risk of dying from breast cancer. This can be accomplished by monthly self-breast exams, annual clinical breast exams and screening mammography. If breast cancer is detected, a multimodality approach incorporating nutritional supplementation, dietary modification, detoxification, and one or more of the following may be considered: surgery, chemotherapy, radiation, hormone therapy, or vaccine therapy.

Life Extension Magazine July, 2009 issue now online

Life Extension magazine July, 2009

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