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口服番茄红素可逆转镉抑制的大鼠体重减轻和脂质过氧化。

Oral administration of lycopene reverses cadmium-suppressed body weight loss and lipid peroxidation in rats.

作者信息

Rencuzogullari Nadir, Erdogan Suat

机构信息

Department of Biochemistry, Faculty of Veterinary Medicine, Mustafa Kemal University, Tayfur Sokmen Campus, Antakya, Hatay, Turkey.

出版信息

Biol Trace Elem Res. 2007 Aug;118(2):175-83. doi: 10.1007/s12011-007-0027-7.

Abstract

Cadmium (Cd) exposure has been recognized to result in a wide variety of cellular responses, including oxidative stress and body weight loss. The aim of the present study was to examine the effect of lycopene supplementation on the antioxidant defense system, lipid peroxidation (LPO) level, nitric oxide (NO), tumor necrosis factor alpha (TNF-alpha) production, and body weight in Cd-exposed rats. Animals were divided into four groups (n = 7): control, Cd-treated, Cd plus lycopene-treated, and lycopene-treated. Cadmium (as CdCl2) was administrated orally for 20 days (6.6 mg kg(-1) day(-1)), and lycopene (10 mg kg(-1) day(-1)) was similarly administered. Lycopene administration significantly suppressed Cd-induced LPO in plasma and kidney homogenates. Lycopene also reversed Cd-decreased body weight compared to the control. Cadmium treatment had diverse effects on the antioxidant enzyme activities. Although antioxidant superoxide dismutase activity was unchanged, glutathione peroxidase activity was decreased, and catalase activity was elevated in kidney homogenates of Cd-administrated group. However, lycopene treatment reversed Cd-changed enzyme activities to the control level. Xanthine oxidase activity and TNF-alpha concentration were not altered by Cd administration, indicating that superoxide anion production and inflammation were not stimulated. Cadmium did not change NO levels in kidney homogenates but decreased those in plasma, and this effect was not prevented by lycopene supplementation. The result suggests that consumption of adequate levels of lycopene may be useful to prevent heavy-metal-induced LPO and body weight loss.

摘要

镉(Cd)暴露已被认为会导致多种细胞反应,包括氧化应激和体重减轻。本研究的目的是检测补充番茄红素对镉暴露大鼠抗氧化防御系统、脂质过氧化(LPO)水平、一氧化氮(NO)、肿瘤坏死因子α(TNF-α)产生及体重的影响。将动物分为四组(n = 7):对照组、镉处理组、镉加番茄红素处理组和番茄红素处理组。口服给予镉(以CdCl2形式)20天(6.6 mg kg-1天-1),同样给予番茄红素(10 mg kg-1天-1)。番茄红素给药显著抑制了镉诱导的血浆和肾脏匀浆中的LPO。与对照组相比,番茄红素还逆转了镉导致的体重下降。镉处理对抗氧化酶活性有不同影响。虽然抗氧化超氧化物歧化酶活性未改变,但谷胱甘肽过氧化物酶活性降低,而镉给药组肾脏匀浆中的过氧化氢酶活性升高。然而,番茄红素处理将镉改变的酶活性逆转至对照水平。镉给药未改变黄嘌呤氧化酶活性和TNF-α浓度,表明超氧阴离子产生和炎症未被刺激。镉未改变肾脏匀浆中的NO水平,但降低了血浆中的NO水平,且补充番茄红素并未阻止这种作用。结果表明,摄入适量的番茄红素可能有助于预防重金属诱导的LPO和体重减轻。

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