Kashka Roya Hedayati, Zavareh Saeed, Lashkarbolouki Taghi
a School of Biology, Damghan University , Damghan , Iran.
b Institute of Biological Sciences, Damghan University , Damghan , Iran.
Syst Biol Reprod Med. 2016 Dec;62(6):404-414. doi: 10.1080/19396368.2016.1235236. Epub 2016 Oct 3.
Cryopreservation-induced oxidative stress (OS) may lead to lipid peroxidation, which may be responsible for decreased cell survival rate. Coenzyme Q10 (CoQ10) as a potent antioxidant may improve cell viability by neutralizing OS. In this study, oxidative lipid injury following the vitrification of preantral follicles was investigated. The effects of CoQ10 treatment on the malondialdehyde (MDA) levels, lipid peroxidation products, and activities of enzymatic and nonenzymatic antioxidants of vitrified preantral follicles were also studied. Preantral follicles were isolated from immature mouse ovaries and were vitrified. After warming, these follicles were cultured with or without CoQ10 for four days. The levels of total antioxidant capacity (TAC) and MDA, as well as the activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT), were assessed at 0, 24, 48, 72, and 96 hours of culture period. The MDA level in the vitrified preantral follicles was higher than that in the fresh groups. By contrast, the MDA level was significantly lower in the groups with CoQ10 treatment than in those without this treatment during cultivation. The TAC level was higher in the fresh preantral follicles than in the vitrified groups. The rates were also higher in the CoQ10-treated groups than in those without this treatment. The activities of SOD, GPX, and CAT were also significantly higher in the fresh groups than in the vitrified groups, especially in the groups with CoQ10 treatment than in those without this treatment. Lowering the vitrification-induced lipid peroxidation of preantral follicles by CoQ10-supplemented maturation medium may be mediated by increasing SOD, GPX, and CAT activities and TAC level during cultivation.
冷冻保存诱导的氧化应激（OS）可能导致脂质过氧化，这可能是细胞存活率降低的原因。辅酶Q10（CoQ10）作为一种有效的抗氧化剂，可能通过中和氧化应激来提高细胞活力。在本研究中，对窦前卵泡玻璃化后的氧化脂质损伤进行了研究。还研究了CoQ10处理对玻璃化窦前卵泡丙二醛（MDA）水平、脂质过氧化产物以及酶促和非酶促抗氧化剂活性的影响。从未成熟小鼠卵巢中分离出窦前卵泡并进行玻璃化处理。解冻后，将这些卵泡在有或没有CoQ10的情况下培养四天。在培养期的0、24、48、72和96小时评估总抗氧化能力（TAC）和MDA水平，以及超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPX）和过氧化氢酶（CAT）的活性。玻璃化窦前卵泡中的MDA水平高于新鲜组。相比之下，在培养过程中，CoQ10处理组的MDA水平显著低于未处理组。新鲜窦前卵泡中的TAC水平高于玻璃化组。CoQ10处理组的比率也高于未处理组。新鲜组中SOD、GPX和CAT的活性也显著高于玻璃化组，尤其是CoQ处理组高于未处理组。补充CoQ10的成熟培养基降低玻璃化诱导的窦前卵泡脂质过氧化可能是通过在培养过程中增加SOD、GPX和CAT活性以及TAC水平来介导的。
