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Updated: Jul 14, 2026
Production and Detection of Reactive Oxygen Species (ROS) in Cancers
Published on: November 21, 2011
Reactive oxygen species in cancer, too much or too little?
1Comprehensive Cancer Center, Columbia University, 630 West 168 Street, New York, NY 10032, USA. fuzy@verizon.net <fuzy@verizon.net>
Abstract:
It is widely accepted that increased levels of reactive oxygen species (ROS) contribute to carcinogenesis. However, this claim has not been confirmed by experiments. On the contrary, a growing number of studies clearly demonstrate that ROS are normal cellular signals and induce cell differentiation and apoptosis, the opposite processes to cancer, which is dedifferentiated. Thus, it is hypothesized here that decreased levels of ROS may lead to cancer development, which is supported by following observations: (1) the fast-growing tumor produces ROS at a rate only one-third of the rate found with the control liver mitochondria; (2) the reduction in tumor mitochondrial content indicates low level of ROS production; (3) the low levels of manganese superoxide dismutase in tumor mitochondria also indicate decreased production of ROS, because the enzyme activity is induced by ROS; (4) lipid peroxidation capacity was decreased in human colon carcinomas and Yoshida hepatomas; (5) low levels of lipid peroxidation de-inhibit glucose-6-phosphate dehydrogenase, whose activity is always increased in a variety of cancers without exception. Clarification of real role of ROS in cancer may shed light on the understanding of how impairment of mitochondria leads to malignant transformation of normal cells, and offer new types of strategies for cancer prevention and therapy.
Insights
Decreased levels of reactive oxygen species (ROS) may cause cancer, contrary to popular belief. Studies show ROS are normal signals, and low ROS levels correlate with tumor growth and cancer development.
Area of Science:
- Biochemistry
- Cell Biology
- Oncology
Background:
- Reactive oxygen species (ROS) are traditionally linked to cancer initiation.
- Emerging evidence suggests ROS act as normal cellular signals, promoting differentiation and apoptosis.
- Cancer is characterized by dedifferentiation, suggesting a potential inverse relationship with ROS levels.
Purpose of the Study:
- To investigate the hypothesis that decreased reactive oxygen species (ROS) levels contribute to cancer development.
- To challenge the conventional view of ROS as solely carcinogenic.
- To explore the role of mitochondria and ROS in malignant transformation.
Main Methods:
- Comparative analysis of ROS production rates in tumor mitochondria versus control liver mitochondria.
- Assessment of mitochondrial content and manganese superoxide dismutase (MnSOD) levels in tumors.
- Measurement of lipid peroxidation capacity in cancerous tissues.
- Evaluation of glucose-6-phosphate dehydrogenase (G6PD) activity in relation to lipid peroxidation.
Main Results:
- Fast-growing tumors exhibited significantly lower ROS production rates compared to controls.
- Reduced mitochondrial content and lower MnSOD levels in tumors indicated decreased ROS production.
- Decreased lipid peroxidation was observed in human colon carcinomas and Yoshida hepatomas.
- Low lipid peroxidation correlated with increased glucose-6-phosphate dehydrogenase activity, a common finding in cancers.
Conclusions:
- The study supports the hypothesis that decreased ROS levels, not increased levels, may drive cancer development.
- Mitochondrial dysfunction and impaired ROS signaling are implicated in cancer's malignant transformation.
- Understanding the true role of ROS could lead to novel cancer prevention and therapy strategies.
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