Albogami Sarah, Hassan Aziza, Ahmed Nibal, Alnefaie Alaa, Alattas Afnan, Alquthami Lama, Alharbi Afaf
Department of Biotechnology, Faculty of Science, Taif University, Taif, Makkah, Kingdom of Saudi Arabia.
Department of Cell Biology, National Research Centre, Dokki, Cairo, Egypt.
PeerJ. 2020 May 21;8:e9232. doi: 10.7717/peerj.9232. eCollection 2020.
Little is known regarding the toxic and therapeutic doses of amygdalin. Treatment regimens and schedules can vary between humans and animal models, and there have been reports of cyanide toxicity due to amygdalin use.
The aim of this study was to evaluate the effect of different doses of amygdalin on antioxidant gene expression and suppression of oxidative damage in mice.
Forty adult male mice were divided randomly into four groups ( = 10) as follows and treated orally for two weeks: a control group treated with saline solution, a group treated with amygdalin at 200 mg/kg body weight, a group treated with amygdalin at 100 mg/kg body weight, and a group treated with amygdalin at 50 mg/kg body weight. Liver and testis samples were collected for gene expression, biochemical and histopathological analyses.
The mice treated with medium-dose amygdalin (100 mg/kg) showed upregulated mRNA expression of glutathione peroxidase ( < 0.01) and superoxide dismutase ( < 0.05) and significantly decreased lipid peroxidation ( < 0.05) in hepatic and testicular tissues compared to those in the untreated groups (controls), with mild histopathological effects. The mice treated with high-dose of amygdalin (200 mg/kg) showed downregulated mRNA expression of glutathione peroxidase and superoxide dismutase ( < 0.01) and significantly increased lipid peroxidation ( < 0.05) in both hepatic and testicular tissues compared to those in the untreated groups (controls), with an apparent effect at the histopathological level. No effects were observed in the mice treated with low-dose amygdalin (50 mg/kg) at the gene, protein and histopathological level.
Low-and medium-dose amygdalin did not induce toxicity in the hepatic and testicular tissues of male mice, unlike high-dose amygdalin, which had a negative effect on oxidative balance in mice. Therefore, amygdalin at a moderate dose may improve oxidative balance in mice.
关于苦杏仁苷的毒性剂量和治疗剂量，人们所知甚少。人类和动物模型的治疗方案和给药时间表可能有所不同，并且有因使用苦杏仁苷导致氰化物中毒的报告。
本研究旨在评估不同剂量的苦杏仁苷对小鼠抗氧化基因表达及氧化损伤抑制的影响。
将40只成年雄性小鼠随机分为四组（每组n = 10），分组如下并进行为期两周的口服给药：用生理盐水处理的对照组、用200 mg/kg体重苦杏仁苷处理的组、用100 mg/kg体重苦杏仁苷处理的组以及用50 mg/kg体重苦杏仁苷处理的组。收集肝脏和睾丸样本用于基因表达、生化及组织病理学分析。
与未处理组（对照组）相比，中等剂量苦杏仁苷（100 mg/kg）处理的小鼠肝脏和睾丸组织中谷胱甘肽过氧化物酶（P < 0.01）和超氧化物歧化酶（P < 0.05）的mRNA表达上调，脂质过氧化显著降低（P < 0.05），组织病理学影响轻微。与未处理组（对照组）相比，高剂量苦杏仁苷（200 mg/kg）处理的小鼠肝脏和睾丸组织中谷胱甘肽过氧化物酶和超氧化物歧化酶的mRNA表达下调（P < 0.01），脂质过氧化显著增加（P < 0.05），在组织病理学水平有明显影响。低剂量苦杏仁苷（50 mg/kg）处理的小鼠在基因、蛋白质和组织病理学水平均未观察到影响。
与高剂量苦杏仁苷不同，低剂量和中等剂量苦杏仁苷未在雄性小鼠的肝脏和睾丸组织中诱导毒性，高剂量苦杏仁苷对小鼠的氧化平衡有负面影响。因此，中等剂量的苦杏仁苷可能改善小鼠的氧化平衡。
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