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Autoinhibitory Feedback Control over Photodynamic Action

机译：光动力作用的自抑制反馈控制

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In biology, the activity of enzymes is usually regulated by feedback loops, which enables direct communication between enzymes and the state of the cell. In a similar manner, with the intention to have automated activity regulation, the therapeutic effect of a photosensitizer (BOD1) is shown to be reduced through a negative feedback loop initiated by the photosensitizer. Photodynamic action produces cytotoxic 1O2 and this reactive oxygen species reacts with ascorbate, generating H2O2. Peroxide-mediated oxidation of the photosensitizer auxiliary group leads to the formation of inactive BOD2 from the parent photosensitizer. BOD1 is shown to accumulate in mitochondria, and cell viability is shown to decrease significantly with BOD1 compared to the loop end product, BOD2. Photoinduced enhancement of fluorescence indicates the formation of inactive BOD2 under cellular conditions, and enhanced fluorescence acts as a reporter for the activity of the photosensitizer. We present the first example of PDT autoinactivation, and such a feedback control mechanism would enable a decrease in post-therapy side effects.
机译：在生物学中，酶的活性通常由反馈环调节，该反馈环可实现酶与细胞状态之间的直接通信。以类似的方式，为了具有自动的活性调节作用，光敏剂（BOD1）的治疗效果显示为通过光敏剂引发的负反馈回路而降低。光动力作用产生细胞毒性的1O2，这种活性氧与抗坏血酸发生反应，生成H2O2。过氧化物介导的光敏剂辅助基团的氧化导致母体光敏剂形成无活性的BOD2。与环终产物BOD2相比，BOD1在线粒体中积累，并且细胞活力显着下降。光诱导的荧光增强表明在细胞条件下无活性BOD2的形成，增强的荧光充当光敏剂活性的报告分子。我们介绍了PDT自动灭活的第一个例子，这种反馈控制机制将能够减少治疗后的副作用。

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