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甲状腺功能减退对家兔脂质过氧化、红细胞抵抗力及血浆抗氧化特性的影响。

Influence of hypothyroidism on lipid peroxidation, erythrocyte resistance and antioxidant plasma properties in rabbits.

作者信息

Brzezińska-Slebodzińska Ewa

机构信息

Department of Hormonal Action Mechanisms, Institute of Animal Reproduction and Food Research of the Polish Academy of Sciences in Olsztyn, 60-166 Poznań, ul. Grunwaldzka 250, Poland.

出版信息

Acta Vet Hung. 2003;51(3):343-51. doi: 10.1556/AVet.51.2003.3.9.

DOI:10.1556/AVet.51.2003.3.9
PMID:14516162
Abstract

The effect of hypothyroidism on some oxidative stress parameters is reported. Moderate hypothyroid state was induced in two groups of female rabbits (3 and 12 months old) by giving 50 mg/kg body weight (BW) of propylthiouracil (PTU) per os for 6 days and 20 mg/kg BW of methimazole (MMI) for further 14 days. Serum T4 and T3 concentrations decreased by about 38-40 and 32-36%, respectively. The induced hypothyroidism resulted in a significant decrease in the serum concentration of the lipid peroxidation end-product malondialdehyde, as measured by the thiobarbituric-acid assay. Erythrocytes of hypothyroid animals exhibited higher resistance to oxidative stress, while submitted to free radicals generator 2,2'-azo-bis(2-amidinopropane) hydrochloride (AAPH) in vitro. Using two detector systems (phospholipid liposomes and deoxyribose), sensitive to either organic or inorganic oxygen radical damage, the ability of euthyroid and hypothyroid rabbit plasma to protect against oxygen radicals was evaluated. The plasma of hypothyroid animals showed about 20% higher ability to protect against iron-binding organic radicals, but about 50% lower chain-breaking antioxidant activity. The antioxidant capacity of plasma against inorganic radicals was not affected by hypothyroidism. In conclusion, the results show that thyroid hormones modulate the free-radical-induced oxidative damage of lipids and that hypothyroidism offers some protection against lipid peroxidation.

摘要

本文报道了甲状腺功能减退对一些氧化应激参数的影响。通过对两组雌性兔子(3个月和12个月大)经口给予50mg/kg体重的丙硫氧嘧啶(PTU),持续6天,随后再给予20mg/kg体重的甲巯咪唑(MMI),持续14天,诱导出中度甲状腺功能减退状态。血清T4和T3浓度分别下降了约38 - 40%和32 - 36%。通过硫代巴比妥酸测定法测量,诱导的甲状腺功能减退导致脂质过氧化终产物丙二醛的血清浓度显著降低。甲状腺功能减退动物的红细胞在体外暴露于自由基发生器2,2'-偶氮双(2-脒基丙烷)盐酸盐(AAPH)时,表现出对氧化应激的更高抗性。使用对有机或无机氧自由基损伤敏感的两种检测系统(磷脂脂质体和脱氧核糖),评估了甲状腺功能正常和甲状腺功能减退兔子血浆对抗氧自由基的能力。甲状腺功能减退动物的血浆对铁结合有机自由基的保护能力高出约20%,但链断裂抗氧化活性低约50%。甲状腺功能减退对血浆对抗无机自由基的抗氧化能力没有影响。总之,结果表明甲状腺激素调节自由基诱导的脂质氧化损伤,并且甲状腺功能减退对脂质过氧化提供了一定的保护作用。

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