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Most of these agents act as inhibitors to affect downstream pro-inflammatory cytokines by blocking the corresponding targets, reducing symptoms and pain ( Figure 1 )
Thus, a potential mechanism underlying paclitaxel-induced chemobrain is the overactivation of intrasynaptic functions ( Similarly, paclitaxel affects synaptic plasticity by increasing presynaptic NMDA receptor (NMDAR) activity, especially that of GluN2A-containing subunits, in the spinal cord, thereby mediating neuropathic pain (Xu et al., 2022)
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Carcinogens such as NNK and PAHs require metabolic activation to exert their carcinogenic effects
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