Monosodium glutamate (MSG) is a major food additive used as a flavor enhancer. A lot of controversies have been generated over the use of MSG. The present study therefore investigated whether MSG would induce cytotoxicity via the induction of mitochondrial permeability transition (mPT) pore opening. 36 male albino rats were used for this study. The rats were equally divided into six groups: group I is the control while group II, III, IV, V, and VI were orally treated with MSG (25, 50, 100, 200, and 400 mg/kg) daily for 28 days. The opening of the pore, cytochrome c release, mitochondrial ATPase activity, mitochondrial lipid peroxidation and hepatic DNA fragmentation were determined spectrophotometrically. Histological assessment of prostate and brain was carried out. The results show that MSG at concentrations ≤30 µg/ml did not induce mPT pore opening while higher concentrations caused significant induction of pore opening. Also, at lower doses (25 and 50 mg/kg), MSG did not cause any significant induction of mPT pore opening while at higher doses, there were significant induction of pore opening. Similar trend of results was recorded for cytochrome c release, mitochondrial ATPase activity and lipid peroxidation. The histological results show that at low doses (25 and 50 mg/kg), no significant lesion was observed while higher doses caused benign prostatic hyperplasia (BPH) in the prostate and necrotic damage in the brain. MSG administration at low dose is tolerable while high doses induce cytotoxicity via mPT pore opening.

味精（MSG）是一种主要的食品添加剂，用作增味剂。关于味精的使用产生了很多争议。因此，本研究调查了味精是否会通过诱导线粒体通透性转变（mPT）孔开放来诱导细胞毒性。本研究使用了 36 只雄性白化大鼠。将大鼠平均分为六组：I组为对照组，II、III、IV、V和VI组每天口服味精（25、50、100、200和400 mg/kg），持续28天。 。通过分光光度法测定孔的开放、细胞色素 c 的释放、线粒体 ATP 酶活性、线粒体脂质过氧化和肝 DNA 碎片。对前列腺和脑进行组织学评估。结果表明，浓度≤30 µg/ml 的味精不会诱导 mPT 孔打开，而较高浓度会显着诱导孔打开。此外，在较低剂量（25 和 50 mg/kg）下，MSG 不会引起任何显着的 mPT 孔打开诱导，而在较高剂量下，则显着诱导孔打开。细胞色素 c 释放、线粒体 ATP 酶活性和脂质过氧化也记录了类似的结果趋势。组织学结果显示，在低剂量（25和50 mg/kg）时，没有观察到明显的病变，而高剂量则引起前列腺良性前列腺增生（BPH）和脑坏死损伤。低剂量的 MSG 给药是可以耐受的，而高剂量的 MSG 通过 mPT 孔开放诱导细胞毒性。