碘酸钾、碘化钾对小鼠脑组织抗氧化能力影响的动态对比研究

目的动态研究不同剂量碘酸钾(KIO3)、碘化钾(KI)对小鼠脑组织抗氧化能力的影响。方法将240只昆明种小鼠按体重随机分为4组(各组浓度以碘离子计):(1)KI 50μg/L剂量组(对照组);(2)KI 180μg/L剂量组;(3)KIO350μg/L剂量组;(4)KIO3180μg/L剂量组。喂养10、20、30周(w)后,检测脑组织匀浆中的谷胱甘肽过氧化物酶(GPx)活性、超氧化物歧化酶(SOD)活性以及丙二醛(MDA)含量。结果与对照组相比,30 w时KI 180μg/L剂量组GPx活性降低(P0.05),SOD/MDA降低(P0.01);30 w时KIO3180μg/L剂量组GPx活性降低(P0.01),SOD/MDA降低(P0.01)。结论 30 w时与对照组相比,KI 180μg/L剂量组与KIO3180μg/L剂量组小鼠脑组织抗氧化能力均有不同程度的降低,其中KIO_3 180μg/L剂量组GPx活性降幅更大。     

现场剂量的不同碘剂对小鼠血液抗氧化能力影响的动态对比研究

目的动态研究现场剂量下碘酸钾(KIO_3)、碘化钾(KI)对小鼠血液抗氧化能力的影响。方法将240只昆明种小鼠按体重随机分为4组(各组浓度以腆含量计):(1)KI 适碘剂量组(K150μg/L);(2)KI 现场剂量组(KI180μg/L);(3)KIO_3适碘剂量组(KIO_350 μg/L);(4)KIO_3现场剂量组(KIO_3180μg/L)。分别喂养10、20、30周(w)后,测定小鼠全血中谷胱甘肽过氧化物酶(GPx)活性、血清中超氧化物歧化酶(SOD)活性以及丙二醛(MDA)含量。结果与KI 适碘剂量组相比,10 w 时其余3组各项指标变化不显著;20 w 时 KIO_3现场剂量组 GPx 活性下降(P<0.05);SOD 活性代偿性增强(P<0.05);30 w 时 KI 现场剂量组 GPx 活性下降(P<0.05);KIO_3适碘剂量组 GPx 活性下降(P<0.01);KIO_3现场剂量组 GPx 活性下降(P<0.01);SOD 活性代偿性增强(P<0.01);MDA 含量增加(P<0.01);SOD/MDA 降低(P<0.05)。结论 30 w 时 KI 现场剂量组与 KIO_3现场剂量组小鼠血液抗氧化能力均有不同程度的降低,其中 KIO_3现场剂量组变化最为显著。     

缺碘大鼠补充不同剂量碘酸钾和碘化钾对甲状腺抗氧化能力的影响

目的观察缺碘Wistar大鼠补充不同剂量碘酸钾(KIO3)和碘化钾(KI)两种碘剂治疗缺碘性甲状腺肿(甲肿)对甲状腺抗氧化能力的影响.方法在成功复制缺碘性甲肿动物模型的基础上,分别给予1倍(适量碘)、5倍和50倍于适量碘的KIO3和KI进行干预性治疗,治疗1个月和3个月后,测定甲状腺组织中的超氧化物歧化酶(SOD)活力以及丙二醛(MDA)含量.结果①6个治疗组的SOD和MDA均明显低于低碘组(LI组),但总体趋势仍高于正常对照组(NI组);②不同补碘剂量之间的比较SOD和MDA在治疗1个月时均随剂量加大呈下降趋势,但在治疗3个月后KIO3组两个指标均随剂量加大呈升高趋势,KI组未发现增高或降低趋势;③不同补碘剂型之间的比较KIO3和KI组在3种碘水平上比较发现,治疗1个月时,KIO3组的SOD均高于KI组,MDA与KI组比较也似有增高趋势;治疗3个月后,KIO3组的SOD与KI组比较似有降低趋势,但MDA似有升高趋势.结论①不同剂量的KIO3和KI均能使缺碘大鼠甲状腺的抗氧化能力得到明显恢复;②短期大剂量KIO3和KI对恢复缺碘大鼠的抗氧化能力效果似较佳,但不宜长期给予;③长期给予适当剂量的KIO3,对恢复缺碘大鼠甲状腺的抗氧化能力与KI组无差别;④适当剂量的KIO3对于纠正碘缺乏是安全有效的.     

碘酸钾和碘化钾对大鼠抗氧化能力和超微结构的影响

目的观察两种碘剂及不同剂量,对大鼠抗氧化能力和超微结构的影响.方法先用低碘饲料和去离子水喂养120只Wistar大鼠3个月复制低碘动物模型.随机分为4组适碘碘酸钾(KIO3)组(NO),适碘碘化钾(KI)组(NI),分别饮含碘量为230μg/L的KIO3和KI去离子水;高碘KIO3组(HO)和高碘KI组(HI)饮水碘含量分别为前2组的100倍.喂养22周后处死,测定甲状腺、视网膜、脑和肾脏的谷胱甘过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、总抗氧化能力(TAOC)和丙二醛(MDA)的含量.光镜和电镜观察脑、视网膜、甲状腺的形态学变化.结果甲状腺NO及HO组GSH-Px活性分别显著低于NI和HI组,NO组SOD活性和HO组TOAC活性分别显著低于NI和HI组;脑NO和HO组GSH-Px、SOD、TOAC组的活性分别显著低于NI和HI组,而MDA的含量则均显著高于NI和HI组,表明KIO3使脑组织多项抗自由基酶活性的损伤,已经进入失代偿阶段;视网膜NO和HO组TOAC的活性均显著低于NI和HI组.形态学观察,光镜下HO、HI组甲状腺滤泡明显增大,上皮细胞多为扁平状,滤泡腔内充满丰富浓染胶质.在电镜下NI组大脑神经元未见异常,NO组神经元胞浆多数粗面内质网(RER)池扩张,核皱缩,树突水肿.HI组神经元有较多呈暗细胞变,RER池扩张,核染色质高度分散均匀.HO组神经元呈高度暗细胞变,胞浆皱缩,RER池扩张,线粒体变性,核内陷.结论相同碘量的生理剂量和大剂量KIO3组抗氧化能力和病理损伤程度比KI组更为严重.NI组损伤的程度为最轻,而HO组则严重.提示,KIO3碘盐防治IDD的安全性,应引起有关方面关注.     

不同剂量碘化钾对大鼠肝脏抗氧化能力的影响

目的观察Wistar大鼠补充不同剂量碘化钾（KI）对肝脏抗氧化能力的影响。方法将Wistar大鼠随机分为6组：低碘组（LI）,适碘组（NI）,5倍高碘组（5HI）,10倍高碘组（10HI）,50倍高碘组（50HI）,100倍高碘组（100HI）。喂养3、6和12个月后,检测肝组织匀浆中的谷胱甘肽过氧化酶（GPx）活性、超氧化物歧化酶（SOD）活性以及丙二醛（MDA）含量。结果LI组GPx活性0.05）。在3和6个月时,4个HI组GPx活性、SOD活性和MDA含量均与NI组无差异（P〉0.05）。但100HI组在实验12个月时GPx活性和SOD活性均较NI组降低（P〈0.05）,而MDA含量无统计学差异（P〉0.05）。结论（1）低碘导致大鼠肝脏抗氧化能力降低;（2）长期摄入高剂量碘未见对肝脏产生明显过氧化损伤,仅于100倍高碘组抗氧化酶活性降低。     

葡萄籽提取物原花青素对糖尿病小鼠的抗氧化作用

目的研究葡萄籽提取物原花青素(GSEP)对糖尿病小鼠抗氧化保护作用的影响。方法以四氧嘧啶小鼠制备糖尿病模型,将造模成功后的小鼠,分为模型组、GSEP低、中、高3个剂量(50、100、150 mg/kg)组,另设正常对照组。连续给药28 d后,空腹12 h后,取全血和肝脏,测定全血和肝组织中超氧歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活力以及丙二醛(MDA)含量。结果经口给予小鼠GSEP 28 d后,高剂量组小鼠全血和肝组织中SOD和GSH-Px活性均明显高于模型组(P<0.05),中、高剂量组小鼠全血和肝组织中丙二醛(MDA)含量均明显低于模型组(均P<0.05)。结论 GSEP对糖尿病小鼠具有明显的抗氧化保护作用。     

白蚁菌圃醇提物的抗氧化作用

目的研究白蚁菌圃醇提物对小鼠的抗氧化作用。方法将50只小鼠分为6组,除正常组(10只)外均每日注射D-半乳糖6 w造成衰老模型。每组随机选取半数小鼠Morris水迷宫定位航行实验,检测全部小鼠血清中超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽(GSH)含量。模型组予不同剂量的白蚁菌圃醇提物灌胃及银杏提取物喂食对照2 w,再次重复检测。结果模型组与正常组比较,Morris水迷宫定位航行实验提示衰老模型组小鼠体力、智力下降;小鼠血清中SOD活性、GSH含量显著降低,MDA量显著升高(P<0.05);而白蚁菌圃醇提物治疗中剂量组与模型组相比较,Morris水迷宫定位航行实验有显著差异(P<0.05);低剂量组小鼠血清中SOD、MDA、GSH含量与模型组相比较有显著差异(P<0.05)。结论白蚁菌圃醇提物可以提高衰老模型小鼠体力和小鼠血清中SOD、GSH,降低MDA含量,具有抗氧化衰老作用。     

β-细辛醚对痴呆小鼠学习记忆能力及SOD、GSH-Px和MDA水平的影响

目的研究β-细辛醚对老年性痴呆小鼠学习记忆能力及血清氧自由基含量的影响。方法以AlCl3痴呆模型小鼠为研究对象,给予不同剂量β-细辛醚,通过水迷宫实验观测小鼠行为学变化和学习记忆能力并检测血清MDA含量、SOD、GSH-Px活性。结果①β-细辛醚组与模型组相比能显著减少游泳时间及错误次数。②模型组与正常组比较,小鼠血清中SOD和GSH-Px活性极显著降低,MDA含量极显著升高(P<0.01);β-细辛醚1.06mg.100g-1.d-1剂量组与正常对照组相比较,血清中SOD、GSH-Px活性,MDA含量变化不显著;β-细辛醚各剂量组与模型组比较有显著差异(P<0.05或P<0.01),但在所设剂量范围内,无剂量依赖性。结论β-细辛醚增强痴呆小鼠学习记忆能力和增高血清SOD、GSH-Px含量,降低MDA含量,可通过调节自由基代谢和提高抗氧化能力发挥易化和增强学习记忆,这可能是其防治老年性痴呆作用机制之一。     

现场剂量不同碘剂致小鼠血细胞DNA损伤的动态观察

目的动态研究现场剂量碘化钾（KI）、碘酸钾（KIO3）对小鼠血细胞DNA损伤情况,进一步探索食盐加碘在剂型、剂量方面的安全性。方法将160只昆明种小鼠,按体重随机分为4组：（1）KI适碘剂量组（I^-50μg/L,正常对照组）;（2）KIO3适碘剂量组（I^-50μg/L）;（3）KI现场剂量组（I^-180μg/L）;（4）KIO3现场剂量组（I^-180μg/L）。喂养20、30周时,每组取材20只,用单细胞凝胶电泳方法观察小鼠血细胞DNA损伤情况。结果 30周与20周相比各组别小鼠血细胞的拖尾均增长;20周时,与KI适碘剂量组相比,各实验组Tail Extent Moment指标差异显著（P〈0.01）;30周时,与KI适碘剂量组相比,各实验组Tail Extent Moment指标差异显著（P〈0.01）。结论在KI、KIO3现场剂量的长期（30周）作用下,可以造成小鼠血细胞DNA损伤。     

山楂对D-半乳糖致衰小鼠抗氧化系统及钙稳态影响的实验研究

目的 观察衰老与细胞内Ca^2 含量的关系和山楂对D-半乳糖衰老小鼠抗氧化作用。方法 本实验以D-半乳糖衰老小鼠为研究对象，分别以大、中、小剂量的山楂水煎剂灌胃45d，测定了青年、老年小鼠血清总抗氧化能力(TAA)，红细胞内超氧化物歧化酶(SOD)活性、脑组织内丙二醛(MDA)含量，红细胞膜Na^ -K^ ATPase，脑组织Ca^2 含量变化，同时，观察不同剂量山楂对老年小鼠上述指标的影响。结果小鼠血清TAA，红细胞内SOD活性，红细胞膜Na^ -K^ -ATPase活性随增龄而下降；脑组织MDA含量，脑组织Ca^2 含量随增龄而上升。山楂可提高小鼠血清TAA，红细胞内SOD活性，红细胞膜Na^ -K^ -ATPase的活性，并能降低脑组织Ca^2 含量，脑组织MDA含量。在各给药组中以山楂中剂量组的抗氧化作用最强。结论 山楂能增强机体抗氧化能力，具有一定的抗衰老作用，同时，脑组织Ca^2 含量可作为衰老的一个指标。     

Potassium Homeostasis

Potassium homeostasis. J. R. Stockigt, Aust. N.Z. J. Med., 1977, 7, pp. 66–77. Potassium balance is regulated by appropriate changes in potassium excretion in the distal portion of the nephron. By contrast, potassium intake, absorption and proximal renal reabsorption do not show regulatory variation. Extracellular potassium concentration, which is a critical factor in membrane polarization, may at times vary in a direction opposite to total body content, because of altered distribution across cell membranes. Alterations in acid-base status frequently disturb homeostasis by altering potassium movement into cells, while insulin has an important regulatory effect on distribution. In general, the multiple renal and extrarenal mechanisms which prevent potassium overload are highly developed, while conservation is relatively ineffective. Consequently, depletion occurs more easily than spontaneous potassium overload. Homeostasis can be disturbed by renal impairment, excessive tissue breakdown, disturbances of acid-base balance, abnormal routes of loss, mineralocorticoid abnormalities and aberrations of sodium balance.     

Potassium in hypertension

Potassium is the most important ion in the living cell, affecting almost every cellular function. Numerous clinical and epidemiologic studies support the knowledge that potassium is a fundamental factor in blood pressure regulation. The role of potassium in blood pressure regulation is reviewed in this article, focusing on its impact on the vascular vessel and the kidney, which are tissues strongly affected by potassium balance. The role of potassium on nitric oxide synthesis and superoxide formation is analyzed. Finally, the study of cell potassium as a marker for hypertension is discussed.     

Potassium replacement therapy

Potassium replacement is often an important therapeutic measure, and the advantages of effervescing potassium-containing granules are put forward in this article.     

Regulation of Potassium Homeostasis

Potassium is the most abundant cation in the intracellular fluid, and maintaining the proper distribution of potassium across the cell membrane is critical for normal cell function. Long-term maintenance of potassium homeostasis is achieved by alterations in renal excretion of potassium in response to variations in intake. Understanding the mechanism and regulatory influences governing the internal distribution and renal clearance of potassium under normal circumstances can provide a framework for approaching disorders of potassium commonly encountered in clinical practice. This paper reviews key aspects of the normal regulation of potassium metabolism and is designed to serve as a readily accessible review for the well informed clinician as well as a resource for teaching trainees and medical students.     

Potassium and the heart

The electrical stability of the heart is more sensitive to the extracellular than to the intracellular potassium concentration. During exercise, extracellular potassium varies rapidly. Catecholamines also modulate the plasma potassium concentration. Hypokalaemia of any cause can precipitate arrhythmias. Ischaemic myocardium loses potassium into the extracellular space within seconds and the cell becomes depolarized. The rise of the extracellular potassium ion concentration accounts for many of the early electrophysiological changes. Abrupt changes of plasma potassium concentration in normal myocardium and a high potassium concentration in ischaemic myocardium can set up electrical forces which initiate arrhythmias. The same phenomenon can account for changes on the electrocardiogram early after the cessation of an exercise test in a patient with ischaemic heart disease. Accumulation of potassium between cells in response to an increase of heart rate is a possible mechanism for false positive exercise tests and Syndrome X.     

Potassium and ventricular arrhythmias

Potassium is a major determinant of the electrophysiologic properties of the myocardial membrane, and it plays an important role in the occurrence of arrhythmia. Hypokalemia has been associated with an increased frequency of ventricular premature complexes (VPCs) in some studies of hypertensive patients treated with diuretics, but other studies have failed to confirm any association. Studies involving patients with an acute myocardial infarction have also provided conflicting data about the association between hypokalemia and VPCs. Whereas the role of potassium in the genesis of simple VPCs remains uncertain, animal and clinical studies have demonstrated a strong relation between hypokalemia and the occurrence of sustained ventricular tachycardia and ventricular fibrillation during acute ischemic states. Hypokalemia may also affect the action of antiarrhythmic drugs by altering the electrophysiologic properties of the myocardium, potentially negating some of the antiarrhythmic activity of these agents. Although diuretic use is the most frequent cause of hypokalemia, epinephrine can also lower serum potassium as a result of stimulation of the beta 2 adrenoreceptor. This mechanism may, in part, explain the ability of beta blockers to prevent sudden death in patients with a recent myocardial infarction.     

Potassium channels and the kidney

Potassium channels play an important role in several renal functions. These include the generation of a cell negative potential in all kidney cells, and potassium channels also participate importantly in the function of the thick ascending limb of Henle's loop and in principal tubule cells of collecting ducts. In the thick ascending limb (TAL), potassium channels mediate recycling of potassium ions across the apical membrane, thereby modulating the turnover of the Na/K/2Cl cotransporter. In the principal tubule cell, potassium channels play a key role in the secretion of potassium. The K channels in both the TAL and cortical collecting duct (CCD) have been cloned, and their functional properties are similar. Hereditary abnormalities of these K channels have been shown to lead to salt loss. Moreover, the delivery of sodium can be shown to be a key determinant of potassium secretion in the terminal nephron segment.