Bharti Vijay K, Srivastava R S
Neurophysiology Laboratory, Division of Physiology & Climatology, Indian Veterinary Research Institute, Uttar Pradesh, India.
Biol Trace Elem Res. 2009 Aug;130(2):131-40. doi: 10.1007/s12011-009-8320-2. Epub 2009 Jan 22.
Fluoride (F) becomes toxic at higher doses and induces some adverse effects on various organs, including brain. The mechanisms underlying the neurotoxicity caused by excess fluoride still remain unknown. The aims of this study were to examine F-induced oxidative stress (OS) and role of melatonin (MEL) and buffalo pineal proteins (PP) against possible F-induced OS in brain of rats. The 24 rats were taken in present study and were divided into four groups: control, F, F + PP, and F + MEL. The F group was given 150 mg/L orally for 28 days. Combined 150 ppm F and 100 microg/kg BW (i.p.) PP and F (150 ppm) + MEL (10 mg/kg BW, i.p.) were also administered. The activities of enzymatic, viz., superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione reductase (GR), and non-enzymatic, viz., reduced glutathione (GSH) concentration, and the levels of malondialdehyde (MDA) in the brain tissue were measured to assess the OS. Fluoride administration significantly increased brain MDA compared with control group, while GSH levels were decreased in fluoride-treated groups, accompanied by the markedly reduced SOD, GPx, GR, and SOD activity. Buffalo PP and MEL administration caused brain MDA to decrease but caused SOD, GPx, GR, GSH, and CAT activities to increase to significant levels in F-treated animals. Together, our data provide direct evidence that buffalo PP and MEL may protect fluoride-induced OS in brain of rats through mechanisms involving enhancement of enzymatic and non-enzymatic antioxidant defense system. Therefore, this study suggested that PP and MEL can be useful in control of neurotoxicity induced by fluoride.
高剂量的氟化物（F）具有毒性，会对包括大脑在内的各种器官产生一些不良影响。过量氟化物导致神经毒性的潜在机制仍然未知。本研究的目的是检测氟诱导的氧化应激（OS），以及褪黑素（MEL）和水牛松果体蛋白（PP）对大鼠脑中可能由氟诱导的氧化应激的作用。本研究选取了24只大鼠，分为四组：对照组、氟组、氟+PP组和氟+MEL组。氟组大鼠口服150 mg/L氟化物，持续28天。同时还给予150 ppm氟化物与100 μg/kg体重（腹腔注射）的PP，以及氟（150 ppm）+MEL（10 mg/kg体重，腹腔注射）。通过测量脑组织中酶促抗氧化剂，即超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPx）、过氧化氢酶（CAT）、谷胱甘肽还原酶（GR）的活性，以及非酶促抗氧化剂，即还原型谷胱甘肽（GSH）的浓度和丙二醛（MDA）的水平，来评估氧化应激。与对照组相比，给予氟化物显著增加了脑MDA水平，而氟处理组的GSH水平降低，同时SOD、GPx、GR和CAT活性明显降低。给予水牛PP和MEL可使氟处理动物的脑MDA水平降低，但使SOD、GPx、GR、GSH和CAT活性增加至显著水平。总之，我们的数据提供了直接证据，表明水牛PP和MEL可能通过增强酶促和非酶促抗氧化防御系统的机制，保护大鼠脑免受氟诱导的氧化应激。因此，本研究表明PP和MEL可用于控制氟诱导的神经毒性。
