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As expected, we detected increased ROS in the presence of IKE, even in cells lacking mitochondria, albeit to a lesser extent compared to mitochondria-replete cells

Nevertheless, this quantitatively smaller intracerebral metabolism is critical for local neurotoxicity because it generates acetaldehyde and ROS in close proximity to neurons and glia

Translating these preclinical findings into clinical applications requires validation of exact molecular mechanisms and dose-response relationships, particularly for H 2 S, to develop targeted therapies for CRC

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