Protective effects of mangafodipir against chemotherapy-induced ovarian damage in mice.
Ying QinAkira IwaseTomohiko Murasenull BayasulaChiharu IshidaNao KatoTomoko NakamuraSatoko OsukaSachiko TakikawaMaki GotoTomomi KotaniFumitaka KikkawaPublished in: Reproductive biology and endocrinology : RB&E (2018)
Oxidative stress might be one of the mechanisms of cisplatin- and paclitaxel-induced the loss of primordial follicles. Mangafodipir can reduce cisplatin- and paclitaxel-induced apoptosis in granulosa cells and primordial follicle activation partially via its SOD activity. At the same time, mangafodipir might have other potential mechanisms to inhibit the activation of primordial follicles. Further, mangafodipir attenuated the ovarian damage caused by cisplatin and paclitaxel without affecting their antitumor activities. Mangafodipir, therefore, though its efficacy might be limited, may be a new option for the preservation of fertility during anticancer treatment.
Keyphrases
- induced apoptosis
- oxidative stress
- chemotherapy induced
- diabetic rats
- endoplasmic reticulum stress
- germ cell
- signaling pathway
- ischemia reperfusion injury
- dna damage
- heat shock
- amyotrophic lateral sclerosis
- insulin resistance
- adipose tissue
- high fat diet induced
- type diabetes
- climate change
- skeletal muscle
- pi k akt
- smoking cessation
- heat shock protein
- human health