Numerous clues link carcinogenesis, tumor biology and metastasis with oxidative stress and antioxidant defense. The two-faced action of reactive oxygen (as well as nitrogen and chlorine) species involves both the induction of DNA damage and intermediacy in intracellular signaling cascades. Both these pathways can favor the induction of cancer. Reactive oxygen species can be involved in initiation and promotion of carinogenesis, activation of proto-oncogenes and inactivation of stability and tumor-suppressing genes. They may oxidatively activate chemical carcinogens. Numerous data document induction of carcinogenesis by chronic active inflammation e. g. due to infection by Helicobacter pylori or Schistosoma haematobium. Oxidative stress has been implicated in the mechanism of cancer induction by ethanol. However, there are also cases in which the level of oxidative damage of DNA is increased but it does not lead to increased carcinogenesis.

Reactive oxygen species enhance the p53 protein activity but increased p53 activity may enhance ROS production. On the other hand, very high levels of ROS inhibit p53. ROS are involved in the action of several proteins involved in the cell cycle regulation. ROS promote apoptosis but their effects are complex and include inactivation of caspases and activation of the Akt pathway promoting cell survival.

ROS may promote metastasis, i. a. by modulating integrin expression and promoting angiogenesis. At least some malignant tumors generate more ROS than normal cells .

Cancers have been reported to have low MnSOD activity and mice heterozygous with respect to MnSOD have increased risk of developing many types of tumors. The same refers to deficiencies in other antioxidant enzymes. However, there are also reports showing that high MnSOD is linked to enhanced tumor invasion, metastasis and poor prognosis.

Chemotherapy has often been associated with oxidative stress. Enhanced antioxidant mechanisms in tumor cells in vivo have been implicated in chemoresistance and leads to poor prognosis, whereas most in vitro studies have reported tumor-suppressing properties of antioxidant enzymes. Dietary or pharmaceutical antioxidant supplementation has been considered a plausible way to prevent ROS-mediated carcinogenicity. However, many antioxidants can act both as antioxidants and prooxidants. Perhaps due to this fact, antioxidant supplementation, though suggested to decrease cancer incidence, lead to equivocal outcome.

In summary, the interaction of oxidative stress and carcinogenesis is an interesting research field still expected to bring results of considerable importance in taming the cancer development.

• Legal notice:
  

  Copyright (c) Pielaszek Research, all rights reserved.
  The above materials, including auxiliary resources, are subject to Publisher's copyright and the Author(s) intellectual rights. Without limiting Author(s) rights under respective Copyright Transfer Agreement, no part of the above documents may be reproduced without the express written permission of Pielaszek Research, the Publisher. Express permission from the Author(s) is required to use the above materials for academic purposes, such as lectures or scientific presentations.
  In every case, proper references including Author(s) name(s) and URL of this webpage: https://science24.com/paper/10976 must be provided.

1. Morphological and functional alterations of A549 cells after treatment with monochloramino acids and hypochlorite
2. The influence of glucose starvation on ferricyanide reduction by Saccharomyces cerevisiae cells
3. Is there any interaction between hydrophilic and hydrophobic antioxidants in the protection against lipid peroxidation in liposomes?