Relevant literatures on the relationship between fluorosis and oxidative stress were reviewed.Based on most of the original papers published in recent years,we can see the increased free radicals and oxidative stress may occur in certain stage of fluoride intoxication,but confirmation of the causality between oxidative stress and fluoride induced damages still remains much work to do.

Objective Recently,it was reported the analy sis of bone free radical by using electron spin resonance (ESR),so this article aimed to determine the changes of bone free radical in fluoresis rats.Methods To analyze the free radical level of bone in fluoresis rats fed with different dose of calcium by ESR method.Results The free radical of bone in the group of low ca lcium level and the group low calcium+fluorides was higher than that in the cont rol group (P<0.01),but that in normal animal feeds (calcium-rich)+fluoride group was lower than that in the control group.Conclusions Low doses of fluoride did not resulted in the increase of free radical in calcium-rich condition at short time,but at low calcium condition,fluoride could increase the level of free radical,these suggested that simple overdose of fluoride did not change the level of free radical of bone.

本实验用常规兔饲料饲养家兔,经饮水投氟复制家兔氟中毒模型,检测了自由基代谢指标,表明红细胞超氧化物歧化酶(Cu-Zn-SOD)、全血谷胱甘肽过氧化物酶(GSH-Px)等抗氧化酶类测定结果,投氟组与对照组间无显著差异.血清脂质过氧化物(LPO)水平高剂量投氟组与对照组未见明显差异,中剂量投氟组较对照组反而降低.用ESR测骨组织的自由基信号,高、中剂量投氟组均显著高于对照组.表明氟中毒时可发生自由基增多.自由基和氧化应激改变与过量氟所致骨相或非骨相损害之间缺乏明确的相关性,目前尚得不出氧化应激参与氟中毒骨病变发生机理的结论.

致心律不齐性右室心肌病(arrhythmogenic right ventricular cardiomyopathy;ARVC)以往也叫右心室发育不良(right ventricular dysplasia;RVD),特点是右室心肌进行性地为纤维脂肪所取代,临床常有心律不齐或猝死.1995年世界卫生组织/国际心肌病学协会(WHO/ISFC)在修订心肌病分类时,将ARVC增列为与扩张性、肥厚性、限制性心肌病并列的第四类心肌病[1].

Objective Study the inhibitory effects of selenium on the production of basic lipid peroxidation and the secretion of extracellular matrix(ECM) of hepatocytes and ito cells in vitro.Methods Rat hepatocytes and ito cells were isolated and cultured.Results The results showed that selenium could obviously lower the production of malondialdehyde(MDA) and raise the activity of glutathione peroxidase(GSH Px) and inhibit the secretion of precollagen type Ⅲ (PCⅢ) in hepatocytes and ito cells as well as inhibit the secretion of hyaluronic acid in ito cells,and that there was a negative correlation between the level of PCⅢ and the ratio of GSH Px/MDA in both cells and a negative correlation between the levels of hyaluronic acid and the ratio of GSH Px/MDA in ito cells.Conclusions These studies indicated that selenium could lower the production of lipid peroxidation and inhibit the secretion of ECMs by raising the activity of GSH Px of rat hepatocytes and ito cells. [

氟骨症这种慢性病程的疾病,尸检材料较难得到,迄今所看到的人体病理材料多系晚期结局.要了解病变的发生发展过程,不得不借助实验病理材料或骨质疏松病人用氟化钠治疗后的髂骨活检材料来补充.

过量氟引起的骨病变中,破骨性吸收占相当重要的位置.虽然过度破骨性吸收是氟骨症致残的一个重要因素,但过量氟对破骨细胞(OC)的作用机制研究却很不充分.本文拟就现有资料对此进行讨论.

目的研究硒(Se)和维生素E(VE)缺乏对大鼠肝细胞的影响.方法以天然低Se低VE的克山病病区粮作为饲料进行动物试验,与人工半合成低Se低VE饲料的实验互相印证;用光镜、电镜、流式细胞术(FCM)、末端脱氧核苷酸转移酶介导的缺口末端标记(TUNEL)、DNA琼脂糖凝胶电泳5种方法进行肝细胞凋亡检测.结果无论天然饲料还是人工半合成饲料实验,低Se低VE组光镜下均可见较多肝细胞胞浆着色深,核浓缩.主要分布在中央静脉周围.电镜检查天然低Se低VE组可见较多肝细胞核体积缩小,核染色质呈块状聚集在核膜下.用流式细胞术检测,天然低Se低VE组较对照组肝细胞凋亡百分率明显增加,补Se和/或VE使调亡百分率有所下降,以联合补充Se和VE凋亡百分率下降最明显.人工半合成饲料低Se低VE组凋亡百分率较高,补Se和/或VE使凋亡百分率有所下降,但均未达到显著差异.无论天然饲料还是人工半合成饲料实验,低Se低VE组均可见较多TUNEL染色阳性细胞,加Se和/或VE可使上述改变的细胞有不同程度减少.DNA琼脂糖凝胶电泳,无论天然还是人工半合成饲料实验低Se低VE组均可见DNA梯状图象,其余各组未见梯状改变.结论Se和VE缺乏可诱导大鼠肝细胞凋亡.

Objective To study whether dietary deficiency of selenium (Se) and vitamine E (VE) can induce hepatocyte apoptosis and what is the role of cAMP and Ca 2+ in the apoptotic process.Methods The experiment was performed on rats kept on natural or semisynthetic diet deficient in Se and VE for 17 weeks.The hepatocyte apoptosis was detected by using flow cytometry in rats.cAMP was detected by using radioimmunoassay,intracellular free Ca 2+ was assayed by fluorescence spectrophotometry after the hepatocytes were loaded with a fluorescence probe (Fura 2AM).Results As compared with Se and VE supplemented groups,hepatocyte apoptosis was obviously increased in rats kept on Se and VE deficient diet,accompanied with an increase of cAMP and Ca 2+ .Conclusions The dietary deficiency of Se and VE can induce hepatocyte apoptosis in rats;cAMP and Ca 2+ may be involved in the regulation of the apoptotic process.

氟化物作为促骨形成药物之一,最早被推荐应用于骨质疏松症的临床治疗,目前仍是唯一可供临床使用的有效的促骨形成的药物.近年来由于成骨细胞(osteoblast OB)培养技术及基因工程技术的发展,对氟化物刺激骨形成作用有了更进一步的认识,有助于我们对氟中毒时氟骨症机制的探讨.

过量氟引起的骨病变复杂多样,涉及参与骨转换的各种细胞,但成骨活跃始终占突出地位.关于氟骨症时骨生成与骨吸收的主、从、先、后,早期文献中曾有不同见解.

<span id="ChDivSummary" name="ChDivSummary" class="abstract-text">采用原位灌注方法分离大鼠肝细胞和储脂细胞 （Ito细胞 ） ,观察微量元素硒 （Se）对CCl4 作用下大鼠肝细胞、Ito细胞细胞外基质 （ECM）产生的拮抗作用。实验结果表明 :Se主要通过提高CCl4 作用下肝细胞、Ito细胞谷胱甘肽过氧化物酶（GPx）活性 ,阻止脂质过氧化损伤 ,继而抑制两种细胞Ⅲ型前胶原 （PCⅢ ）分泌以及Ito细胞EMG的分泌</span>

Objective To study whether dietary deficiency of selenium (Se) and vitamine E(VE) can induce hepatocyte apoptosis and what is the role of p53,bcl-2 and c-myc in the apoptotic process.Methods The experiment was performed on rats kept on natural or semisynthetic diet deficient in Se and VE for 17 weeks.The hepatocyte apoptosis was detected by using TUNEL in rats.The p53,bcl-2 and c-myc proteins were detected by immunohistochemistry in hepatocytes.Results As compared with Se and VE supplemented group,hepatocyte apoptosis was obviously increased in rats kept on Se and VE deficient diet,accompanied with an increased expression of p53 and c-myc protein but a lower expression of bcl-2 protein in hepatocytes.Conclusions The dietary deficiency of Se and VE can induce hepatocyte apoptosis in rats;p53,bcl-2 and c-myc may be involved in the regulation of the apoptotic process.

目的研究氟化物对肝细胞凋亡的影响.方法用偏食饲料、饮水加氟化钠100mg/L或同时加碳酸钙3 200mg/kg饲料喂饲大鼠2个月,用流式细胞术检测肝细胞凋亡小体百分率,同时检测了谷胱苷肽过氧化物酶活性和脂质过氧化物含量.结果发现氟中毒组大鼠肝细胞凋亡小体百分率较对照组明显升高(P=0.01～0.05),加钙可使这种改变更为明显(P<0.01);而GSH-px活性则明显降低.结论氟化物的毒性可导致肝细胞凋亡,对机体抗氧化能力的降低可能起一定作用.

为研究低钙动物的生长代谢及与疾病的关系.介绍一种可行的不同血钙水平大鼠动物模型,通过控制膳食内钙水平对所饲大鼠血钙进行调节.用Wistar大鼠,按体重和性别均匀分层分为7组.所用的基础LC饲料,是以玉米面为主的膳食配方所配成,其中低钙特点突出,所饲大鼠血钙水平明显低下,体重生长迟缓、代谢偏低.研究结果表明,LC组大鼠血清Ca水平仅及Stock组一半,体重增长迟缓,当膳食补Ca后,血Ca水平随补Ca量逐渐升高,而体重增长也随之变化升高,呈明显的量效关系,LC+600Ca组血Ca接近正常水平.当膳食内总钙在1000mg/kg时,即LC+600mg/kg组,上述生长迟缓的状态即被改善,P＜0.01.

OBJECTIVE:To examine the relationship between selenium (Se)- and vitamin E(VE)-deficiency and thyroid hormone (TH) metabolic disturbance, especially type I iodothyronine 5'-deiodinase (ID-I) activity.METHODS:We observed the metabolic changes of TH-3, 3',5-triidothyronine (T3) and thyroxin (T4) and their free radicals-glutathione peroxidase (GSH-Px) and lipid peroxides (LPO) in the peripheral tissues (liver, kidney and blood) of Wistar rats maintained on Se- and VE-deficient artificial semi-synthetic diet for 8 weeks.RESULTS:In the Se- and VE-deficient rats (compared with Se- and VE-supplement rats): 1). Hepatic and renal ID-I activities decreased by 60% and 50% respectively, serum levels of T3 reduced 36%, and T4 increased by 32%. Hepatic ID-I activity and serum T3 concentration in Se- and VE-supplement rats were significantly higher than those in the Se-supplement and VE-deficient rats. 2). GSH-Px activities in the whole blood and liver decreased by 61% and 82% respectively. LPO concentrations in serum and liver increased by 53% and 40% respectively. When Se content remained the same, changes of VE content did not significantly affect GSH-Px activity, but the combined supplement of Se and VE decreased significantly the LPO concentration.CONCLUSIONS:The data suggests that GSH-Px activity is influenced mainly by Se level, but ID-I activity is influenced by VE concentration in addition to Se level. VE seemed to play a protective role on ID-I and its mechanism might be related to the fact that VE protects the stability of microsomal membrane in which ID-I exists, avoiding from free radical damage as well as the coordinated action and mutual sparing effect of Se and VE.

克山病是一种地方病。地方病可由各种原因引起。从病理形态分析认为本病可能是由于某种化学物质中毒或某种营养素缺乏所致。因而我们愿着重从生物地球化学方面探讨病因。关于克山病流行区的地球化学特点,目前还缺乏全面、精细的资料。根据现有初步分析结果来看,患区土壤和水的化学组成确有一些异常,其中钡的过多问题引起了我们的注意。于是我们便进行了慢性钡中毒的