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Xenobiotics, Oxidative Stress, and Antioxidants

Call for Papers

Xenobiotics such as drugs, chemotherapy, food additives, and environmental pollutants are foreign chemical compounds to our biological system. These compounds generate several free radicals that lead to increase the oxidative stress in the cells. Accumulation of oxidative stress in the cells leads to significant increase in the cellular reduction potential and may result in reducing capacity of the cellular redox couples. The formation of considerable amounts of reactive oxygen species (ROS) is responsible for induction of many diseases including aging, diabetes, cardiovascular disease, cancer, immune function, metabolism, and neurodegeneration. On the other hand, antioxidants are beneficial components that neutralize free radicals before they interact with the cell components and prevent the oxidative damage to the cells. There is a strong evidence supported the notion that dietary antioxidants are useful protectors against oxidative stress and play an important role in preventing human diseases. The oxidative stress is a condition of imbalance between ROS generation and cellular antioxidant capacity. The accumulation of generated ROS in the cells leads to dysfunction of the antioxidant system. The new insights of cellular and molecular mechanisms of contribution of oxidative stress in several organ systems and the methods as well as the markers used for its evaluation will be discussed.

Potential topics include but are not limited to the following:

  • Toxicity of xenobiotics
  • Role of redox-related processes in the metabolism and detoxification of xenobiotics
  • Role of xenobiotics in prompt diseases development
  • Effects of xenobiotics on redox system at the cellular and molecular level in animal and/or human studies
  • Role of antioxidants in alleviating xenobiotics toxicity

Authors can submit their manuscripts through the Manuscript Tracking System at

Manuscript DueFriday, 30 June 2017
First Round of ReviewsFriday, 22 September 2017
Publication DateFriday, 17 November 2017

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