International journal of radiation biology · 2026
Radiomodulatory effects of rosmarinic acid in melanocytic cells.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Olivares Amparo, Mercado Ana María, Achel Daniel Gyingiri, García-Gamuz José Antonio, Castillo Julián, Alcaraz Miguel
Аннотация
MATERIALS AND METHODS: Four cell lines with differing degrees of radiosensitivity were employed: PNT2 (non-tumoral prostate epithelial cells used as reference), MELAN A (normal murine melanocytes), SK-MEL-1 (human metastatic melanoma cells), and B16F10 (murine metastatic melanoma cells). Cell survival assays, apoptosis, intracellular glutathione status, and cell cycle progression were evaluated 48 hours following exposure to 20 Gy X-rays, with or without RA pretreatment at 25 µM administered 15 minutes before irradiation.
RESULTS: In PNT2 cells, RA conferred robust radioprotection with a protection factor of 99 ± 1.0% (p < .001), reducing radiation-induced apoptosis by more than 300%, significantly increasing the GSH/GSSG ratio, and normalizing cell cycle distribution. In MELAN-A and SK-MEL-1 cells, RA abolished radioprotection, reduced the GSH/GSSG ratio, and increased the apoptotic fraction. In B16F10 cells, RA tripled radiation-induced cell death (p < .001), further depleted the GSH/GSSG ratio, increased apoptosis, and markedly aggravated G2/M arrest, demonstrating a frank and significant radiosensitizing effect. The loss of radioprotective capacity is: B16F10 > Melan-A = SK-MEL-1 > PNT2 (p < .001).
CONCLUSIONS: RA exhibits a cell-type-dependent radiomodulatory profile: it effectively protects normal epithelial cells while losing its radioprotective capacity-or acting as a radiosensitizer-in melanin-producing cells. Confirmation of this selectivity in vivo studies could represent a promising strategy to widen the therapeutic window in melanoma radiotherapy.
RESULTS: In PNT2 cells, RA conferred robust radioprotection with a protection factor of 99 ± 1.0% (p < .001), reducing radiation-induced apoptosis by more than 300%, significantly increasing the GSH/GSSG ratio, and normalizing cell cycle distribution. In MELAN-A and SK-MEL-1 cells, RA abolished radioprotection, reduced the GSH/GSSG ratio, and increased the apoptotic fraction. In B16F10 cells, RA tripled radiation-induced cell death (p < .001), further depleted the GSH/GSSG ratio, increased apoptosis, and markedly aggravated G2/M arrest, demonstrating a frank and significant radiosensitizing effect. The loss of radioprotective capacity is: B16F10 > Melan-A = SK-MEL-1 > PNT2 (p < .001).
CONCLUSIONS: RA exhibits a cell-type-dependent radiomodulatory profile: it effectively protects normal epithelial cells while losing its radioprotective capacity-or acting as a radiosensitizer-in melanin-producing cells. Confirmation of this selectivity in vivo studies could represent a promising strategy to widen the therapeutic window in melanoma radiotherapy.