Abstract
Oxidative stress plays an important role in cellular processes. Consequently, oxidative stress also affects etiology, progression, and response to therapeutics in various pathological conditions including malignant tumors. Oxidative stress and associated outcomes are often brought about by excessive generation of reactive oxygen species (ROS). Accumulation of ROS occurs due to dysregulation of homeostasis in an otherwise strictly controlled physiological condition. In fact, intracellular ROS levels are closely associated with the pathological status and outcome of numerous diseases. Notably, mitochondria are recognized as the critical regulator and primary source of ROS. Damage to mitochondria increases mitochondrial ROS (mROS) production, which leads to an increased level of total intracellular ROS. However, intracellular ROS level may not always reflect mROS levels, as ROS is not only produced by mitochondria but also by other organelles such as endoplasmic reticulum and peroxisomes. Thus, an evaluation of mROS would help us to recognize the biological and pathological characteristics and predictive markers of malignant tumors and develop efficient treatment strategies. In this review, we describe the pathological significance of mROS in malignant neoplasms. In particular, we show the association of mROS-related signaling in the molecular mechanisms of chemically synthesized and natural chemotherapeutic agents and photodynamic therapy.
Highlights
Reactive oxygen species (ROS) are intracellular signaling molecules formed by the reduction of O2, and include superoxide anion (O2 − ), hydrogen peroxide (H2 O2 ), as well as hydroxyl radicals (OH) [1].Under normal physiological conditions, this substance participates in the maintenance of metabolic homeostasis, and exhibits regulatory roles in proliferation and differentiation [2,3,4]
This study showed that Mitochondrial ROS (mROS) production increased in a Tannic acid (TA) concentration-dependent manner, and Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated extrinsic apoptosis pathway was activated in response to mROS generation [110]
The methodology employed in this study was as follows: First, F9 cells were established from a clonal mouse teratocarcinoma and, second, mitochondrial oxidative stress was induced by sodium fluoride (NaF)
Summary
Reactive oxygen species (ROS) are intracellular signaling molecules formed by the reduction of O2 , and include superoxide anion (O2 − ), hydrogen peroxide (H2 O2 ), as well as hydroxyl radicals (OH) [1]. 2 of 20 and metabolic signaling [10] They are recognized as a major source of ROS, and mitochondria-derived. Are tightlyare regulated in the Mitochondrial playincrucial roles inand various metabolic signaling [10] They are recognized as a major source of ROS, and mitochondriabiological activities including cell differentiation, survival, and immunity, and can accumulate upon derived ROS (mROS) are tightly regulated in the cell. In various biological activities including cell differentiation, survival, and immunity, and can Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) are a major source accumulate upon mitochondrial dysfunction, imbalance of antioxidant homeostasis, and/or hypoxic of ROS [12]. There is aproduction general agreement that mitochondria and NOXs are the major sources of molecules are associated with intracellular production by complex mechanisms. We believe that deciphering the specific roles and regulative mechanisms of mROS production is essential to develop patient-specific treatment strategies for cancer
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