Oxidative stress in environmental-induced carcinogenesis

Area of Science:

• Biochemistry
• Pathophysiology
• Oncology

Background:

• Reactive oxygen species (ROS) are natural free radicals implicated in tissue injury from various sources like xenobiotics and UV exposure.
• Oxidative stress arises from an imbalance between ROS production and the body's detoxification or repair mechanisms.
• This stress is a critical factor in the pathophysiology of common human diseases, notably cancer.

Purpose of the Study:

• To elucidate the role of oxidative stress in the development of human pathologies, with a focus on cancer.
• To highlight the mechanisms by which ROS contribute to cellular damage, including DNA mutations.
• To emphasize the interconnectedness of oxidative stress, inflammation, senescence, and cancer.

Main Methods:

• Literature review and synthesis of existing research on reactive oxygen species and oxidative stress.
• Analysis of the molecular mechanisms linking ROS to cellular damage (protein, lipid, DNA).
• Examination of etiological factors contributing to oxidative stress and their procarcinogenic potential.

Main Results:

• ROS are identified as significant contributors to tissue injury and disease pathogenesis.
• Oxidative stress directly causes DNA damage, including base oxidation and mutations, which are hallmarks of malignant tumors.
• Various lifestyle and environmental factors, alongside aging and obesity, promote carcinogenesis via oxidative stress.

Conclusions:

• Oxidative stress is a central pathophysiological mechanism in many human diseases, particularly cancer.
• ROS-induced DNA damage and mutations are critical steps in cancer development.
• Oxidative stress, inflammation, senescence, and cancer are interconnected concepts requiring a coordinated approach for understanding and treatment.