Cell Stress Chaperones. 2008;13:31
Prevention of chemotherapy-induced alopecia in rodent models.
Jimenez JJ, et al
…..Next, we tested whether the same protective mechanism could also mitigate or suppress the alopecic effects of anthracyclines, alkylating agents, and taxanes. Groups of (typically four) animals were subjected to heat treatment to the nape of the neck or were not heat-treated. After a delay of 7 h, the groups were administered alopecia-causing doses of cyclophosphamide or a combination of cyclophosphamide and adriamycin. Because no alopecia-causing, sublethal i.p. dose of taxol could be identified, amounts sufficient to cause local hair loss were injected s.c. in the region that had previously been subjected to heat treatment. Results summarized in Table 2 indicated that hair in heat-treated areas was effectively protected against the latter antineoplastic agents. No protection was observed in unheated, drug-exposed animals. Subcutaneous injection of GA also prevented hair loss caused by cyclophosphamide and taxol. Following standard practice in the field, we had observed and recorded protective effects at the time animals had lost most of their body hair, which occurred about 1 week after exposure to chemotherapeutic agents. Anticipating a potential future use of the same preventative method in human patients, we investigated whether the observed protective effects were long-lasting. We followed-up heat-preconditioned, chemotherapeutic drug-treated (etoposide, cyclophosphamide, or cyclophosphamide/adriamycin) animals for longer periods, in some cases, until they had acquired a new fur coat about 3 weeks after chemotherapy. We observed that a majority of animals, and in some groups, all animals exposed to 48–48.5°C heat for 20 min retained their patches of protected hair. However, at lower heat doses, animals tended to gradually lose their patches.
Edited for Hair regrowth blog use.