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ROS-Mediated Selective Killing Effect of Black Phosphorus: Mechanistic Understanding and Its Guidance for Safe
Na Kong1, Xiaoyuan Ji1, Junqing Wang1
1Center for Nanomedicine and Department of Anesthesiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, United States.
Abstract:
Black phosphorus (BP)-based nanomaterials have distinguished advantages and potential applications in various biomedical fields. However, their biological effects in physiological systems remain largely unexplored. Here, we systematically revealed a reactive oxygen species (ROS)-mediated mechanism for the selective killing of cancer cells by BP-based nanosheets. The treatment with BP-based materials can induce higher levels of ROS in cancer cells than in normal cells, leading to significant changes in the cytoskeleton, cell cycle arrest, DNA damage, and apoptosis in tumor cell lines. We revealed that the decreased superoxide dismutase activity by lipid peroxides could be an essential mechanism of the selectively higher ROS generation induced by BP-based nanosheets in cancer cells. In addition, the selective killing effect only occurred within a certain dosage range (named "SK range" in this study). Once exceeding the SK range, BP-based materials could also induce a high ROS production in normal tissues, leading to detectable DNA damage and pathological characteristics in normal organs and raising safety concerns. These findings not only shed light on a new mechanism for the selective killing of cancer cells by BP-based materials but also provide deep insights into the safe use of BP-based therapies.
Insights
Black phosphorus (BP) nanosheets selectively kill cancer cells by inducing reactive oxygen species (ROS). However, exceeding a specific dose range can harm normal tissues, highlighting the need for careful application in biomedical therapies.
Area of Science:
- Biomedical Engineering
- Materials Science
- Oncology
Background:
- Black phosphorus (BP)-based nanomaterials show promise in biomedicine.
- Their biological effects and mechanisms, especially in cancer therapy, are not fully understood.
Purpose of the Study:
- To elucidate the mechanism behind the selective killing of cancer cells by BP-based nanosheets.
- To investigate the role of reactive oxygen species (ROS) in this process.
- To determine the safety profile and dosage limitations of BP-based nanomaterials in vivo.
Main Methods:
- Systematic investigation of BP-based nanosheets' effects on cancer and normal cells.
- Measurement of ROS levels, superoxide dismutase activity, and lipid peroxidation.
- Analysis of cellular responses including cytoskeleton changes, cell cycle arrest, DNA damage, and apoptosis.
- Evaluation of pathological changes in normal organs at different dosages.
Main Results:
- BP-based nanosheets induce higher ROS levels in cancer cells than normal cells, leading to cancer cell death.
- Decreased superoxide dismutase activity due to lipid peroxides is a key mechanism for selective ROS generation in cancer cells.
- A specific dosage range (SK range) is critical for selective cancer cell killing; exceeding this range causes ROS production and damage in normal tissues.
Conclusions:
- BP-based nanosheets offer a novel ROS-mediated mechanism for selective cancer cell killing.
- Understanding the "SK range" is crucial for safe and effective application of BP-based therapies.
- These findings provide critical insights for the development of safe BP-based biomedical applications.
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