Free Radicals in Cancer

28th Tuesday, 2012  |   Others  |  no comments

Oxygen is a highly reactive atom that is capable of becoming part of potentially damaging molecules commonly called “ free radicals.” Free radicals are capable of attacking the healthy cells of the body, causing them to lose their structure and function. Free radicals are electrically charged molecules, i.e., they have an unpaired electron, which causes them to seek out and capture electrons from other substances in order to neutralize themselves. The formation of free radical is chain reaction and until subsequent free radicals are deactivated, thousands of free radical reactions can occur within seconds of initial reaction. Cells in humans and other organisms are constantly exposed to a variety of oxidizing agents and these may be present in air, food, and water, or they may be produced by metabolic activity within cells. The key factor is to maintain a balance between oxidants and antioxidants to sustain optimal physiological conditions. Overproduction of oxidants can cause an imbalance, leading to oxidative stress, especially in chronic bacterial, viral, and parasitic infections (Ames et al. 1993a, 1993b). Oxidative stress can causeoxidative damage to large biomolecules, such as lipids, proteins, and DNA, resulting in an increased risk for cancer and Cardiovascular diseases (Ames et al. 1993a).
Reactive oxygen species (ROS) is a term, which encompasses all highly reactive, oxygen-containing molecules, including free radicals. Types of ROS include the hydroxyl radical, superoxide anion radical, hydrogen peroxides, singlet oxygen, nitric oxide radical, hypochlorite radical, and various lipid peroxides. Free radicals can react with membrane lipids, nucleic acids, proteins and enzymes, and other small molecules, resulting in cellular damage and finally leads to cancer (Fig. 16.1). ROS are generated by a number of pathways. Most of the oxidants produced by cells occur as:
1. A consequence of normal aerobic metabolism: approximately 90% of the oxygen utilized by the cell is consumed by the mitochondrial electron transport system.
2. Oxidative burst from phagocytes (which blood cells) as part of the mechanism by which bacteria and viruses are killed, and by which foreign proteins (antigens) are denatured.
3. Xenobiotic metabolism, i.e.,detoxification of toxic substances
The term” oxidative stress” has been coined to represent a shift towards the pro-oxidants in the pro-oxidant/antioxidant balance that can occur as a result of an increase in oxidative metabolism. Increased oxidative stress at the cellular LEVEL is mainly due to factors such as exposure to alcohol, medications, trauma, cold, infections, poor diet, toxins, radiation, or strenuous physical activity etc. Oxidative damage to DNA, proteins, and other macromolecules has been implicated in the pathogenesis of a wide variety of diseases, such as heart disease and cancer (Halliwell 1994).
The reactive oxygen species (ROS) can damage the nucleic acids. The oxidative modification of the DNA constitutes the fundamental molecular event in carcinogenesis (Trueba et al. 2004). Oxidative DNA damage-induced mutagenesis is widely hypothesized to be a frequent event in the normal human cell. The enormous evidence suggests an important role of ROS in the expansion and progression of tumor clones, being considered a relevant class of carcinogens

) It’s also a violation of his rights

26th Sunday, 2012  |   Uncategorized  |  no comments

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Don’t miss the craft table sale filled with holiday gifts

24th Friday, 2012  |   Uncategorized  |  no comments

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Regression of prostate cancer following administration of Genistein Combined Polysaccharide (GCP), a nutritional supplement: a case report

21st Tuesday, 2012  |   Prostate Cancer  |  no comments

It has been reported that genistein, an isoflavone used in soybeans, has antiprostate cancer effects. Genistein Combined Polysaccharide (GCP trade mark; AMino Up, Sapporo, Japan), a nutritional supplement manufactured in Japan, is composed of genistein and a polysaccharide obtained from basidiomycetes (mycelia) that grows in a variety of mushrooms.
We report a case of a patient with a biopsy proven prostate cancer showing clinical and pathologic evidence of regression following administration of GCP. The patient was enrolled in an Institutional Review Board (IRB)-approved protocol and received GCP for 6 weeks prior to radical prostatectomy.
The patient’s prostate-specific antigen (PSA) decreased from an initial value of 19.7 to 4.2 ng/mL after 44 days of low-dose GCP. No cancer was identified in the radical prostatectomy specimen and no side effects were observed in this patient.
This case suggests that GCP, which has shown potent inhibitory effects against prostate cancer in vitro, may have some potential activity in the treatment and prevention of prostate cancer.
Source:
Ghafar MA, Golliday E, Bingham J, et al. J Altern Complement Med. 2002 Aug;8(4):493-7.

Genistein inhibits the stemness properties of prostate cancer cells through targeting Hedgehog–Gli1 pathway

21st Tuesday, 2012  |   Prostate Cancer  |  no comments


Cancer stem cells (CSCs) are involved in tumorigenesis and progression of prostate cancer (PCa). Conventional anticancer therapeutics failed to eradicate CSCs, which may eventually lead to the disease relapse and metastasis. Therefore, targeting prostate CSCs may be an ideal strategy to cure PCa. Genistein is a major isoflavone constituent of soybeans and soy products, which has been shown to exhibit potent anticancer effect on many cancers. We have previously reported that genistein can inhibit PCa cell invasion by reversing epithelial to mesenchymal transition, suggesting that genistein may be effective against metastatic PCa. In addition, we have recently demonstrated that PCa tumorsphere cells (TCs) possess CSC properties. Here, we found that tumorsphere formation and colony formation of Pca cells were noticeably suppressed in the presence of genistein. Pretreatment of PCa TCs with genistein also suppressed tumorigenicity in vivo. Additionally, genistein treatment inhibited tumor growth of PCa TCs. Further studies showed that genistein treatment not only led to the down-regulation of PCa CSC markers CD44 in vitro and in vivo, but also inhibited Hedgehog–Gli1 pathway, which may contribute to the anti-CSC effect of genistein in PCa TCs. Therefore, our findings demonstrated that genistein may be a dietary phytochemical with potential to target prostate CSCs.
Source:
Zhang L, Li L, Jiao M, Wu D, et al. Cancer Letters. Volume 323, Issue 1, 1 October 2012, Pages 48–57