The Scientific World Journal

Toxicology and Disease/Cancer Therapy in Reactive Oxygen Species-Mediated Drugs and Treatments

Publishing date
20 Feb 2015
Submission deadline
03 Oct 2014

Lead Editor

1Kaohsiung Medical University, Kaohsiung, Taiwan

2University of Louisville, Louisville, USA

3I-Shou University, Kaohsiung, Taiwan

4SK University of Agricultural Sciences and Technology, Chatha, India

Toxicology and Disease/Cancer Therapy in Reactive Oxygen Species-Mediated Drugs and Treatments


Many anticancer agents and/or natural products may modulate the level of reactive oxygen species (ROS) and induce or protect cellular oxidative damage. ROS has also been reported to be involved in apoptosis, autophagy, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, cell migration, and invasion. Although many ROS modulating drugs affect the proliferative ability of cancer cells, they may also generate various side effects on normal cells. Accordingly, the toxicology and disease/cancer therapy in ROS-mediated drugs and treatments are still challenging.

The overall aim of this special issue is to present the recent advances in both benefit and side effects and signaling mechanisms for anticancer and disease therapeutic drugs and/or natural products based on their ROS modulation ability. Furthermore, the aim of this issue also provides the innovative reviews of the features of ROS modulation of anticancer and disease therapeutic drugs and/or natural products in cell-based studies, animal model, and clinical application.

We invite investigators to contribute original research articles as well as review articles that will stimulate the continuing efforts on exploring the ROS modulating effects and downstream signaling mechanisms for ROS-mediated drugs and/or natural products for drug chemoprevention, chemotherapy, and disease therapy, as well as the emerging pharmacogenomics issues. ROS modulating effects of drugs on noncancer diseases, antibacteria, and antivirus are also welcome.

Potential topics include, but are not limited to:

  • Anticancer drugs
  • Natural products
  • Toxicology
  • ROS
  • RNS
  • Signal transduction
  • Apoptosis
  • Autophagy
  • Endoplasmic reticulum (ER) stress
  • DNA damage
  • DNA repair
  • Bioassay
  • Chemical engineering
  • Antioxidant
  • Chemoprevention
  • Chemotherapy
  • Single nucleotide polymorphism (SNP)
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