Reversible inhibition of mammalian tubulin assembly <i>in vitro</i> and effects in <i>Saccharomyces cerevisiae</i> D61.M by mitomycin C

Albertini, Silvio; Friederich, U.; Würgler, Friedrich E.

doi:10.1093/mutage/4.1.39

Cited by 5 publications

(1 citation statement)

References 11 publications

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“…These platinum compounds cause deacetylation of alpha-tubulin and hyperphosphorylation of microtubuleassociated protein tau (143). Mitomycin C and etoposide have also been shown to affect tubulin (144,145). Yokomizo et al have shown that these four important chemotherapies, doxorubicin, cisplatin, mitomycin C and etoposide, increase superoxide anions, while tubulin inhibitors (vincristine) do not (146).…”

Section: Tubulin Inhibitors and Other Chemotherapiesmentioning

confidence: 99%

The Mystery of Chemotherapy Brain: Kynurenines, Tubulin and Biophoton Release

Sordillo

2020

Anticancer Res

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The majority of patients receiving chemotherapy experience post-chemotherapy cognitive impairment, sometimes referred to as "chemo brain" or "chemo fog." The cognitive impairment associated with this syndrome can be severe, and can sometimes last for many years after therapy discontinuation. Despite extensive investigations, its etiology is unknown. We argue that chemo brain results from damage to tubulin within microtubules. This damage can occur directly from tubulin inhibitors such as taxanes, epothilones or vinca alkaloids. Other chemotherapies stimulate increased mitochondrial activity and biophoton release. This results in abnormal tryptophan metabolism and excess production of neurotoxic kynurenines, which, in turn, damage microtubules.

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Section: Tubulin Inhibitors and Other Chemotherapiesmentioning

confidence: 99%