. 2024 Oct 15;16(10):6064–6071. doi: 10.62347/WOXO2630

Table 6.

Mechanisms of peripheral nerve tissue damage associated with cosmetic-related mercury poisoning

Nerve injury	Potential mechanism
Pain	Activation of glial cells leads to the release of proinflammatory cytokines and other active substances. These factors interact with neurons, facilitating the transmission and progression of neuropathic pain [43,44].
Aging	Methylmercury impairs neurons by blocking e2-tubulin, disrupting the internal structure and biochemical balance of neurons. This interference affects cell growth, differentiation, and survival through the PKC cascade, ultimately leading to abnormal energy metabolism, impaired mitochondrial function, and disrupted signal transmission. Over time, these effects contribute to accelerated neuronal aging [45,46].

Nerve injury

Potential mechanism

Pain

Activation of glial cells leads to the release of proinflammatory cytokines and other active substances. These factors interact with neurons, facilitating the transmission and progression of neuropathic pain [43,44].

Aging

Methylmercury impairs neurons by blocking e2-tubulin, disrupting the internal structure and biochemical balance of neurons. This interference affects cell growth, differentiation, and survival through the PKC cascade, ultimately leading to abnormal energy metabolism, impaired mitochondrial function, and disrupted signal transmission. Over time, these effects contribute to accelerated neuronal aging [45,46].