缺血与再灌注对大鼠肾脂质过氧化物含量和钠,钾浓度的影响

本研究用成年雄性Wistar大鼠,作肾缺血和再灌注实验;发现:(1)缺血60分钟组的肾皮质脂质过氧化物含量(MDA76.05±18.14nmol/g)显著降低(P<0.001),钠浓度(97.43±10.20mEq/L)显著增高(P<0.01)而钾浓度(74.68±6.36mEq/L)显著降低(P<0.002)。(2)缺血60分钟再灌注30分钟组的肾皮质,脂质过氧化物含量(147.25±17.18nmol/g)显著增加(P<0.01),钠、钾浓度接近正常值(79.61±18.44和90.33±6.13mEq/L)。缺血与缺血再灌注肾皮质其脂质过氧化物含量同钠钾浓度之间无显著相关。实验提示:(一)缺血再灌注肾氧自由基“爆发性”生成所引发的脂质过氧化可能是肾缺血后损伤的重要机制之一。(二)缺血肾内钠、钾浓度变化似能反映缺血引起的细胞膜钠泵失灵及细胞内外离子分布异常。这种变化同氧自由基生成和脂质过氧化强度之间,似无直接因果关系。     

X线对仔鼠胃组织结构及总抗氧化能力、谷胱甘肽过氧化物酶和谷胱甘肽还原酶活性的影响

目的 观察X线辐射后仔鼠胃组织结构和总抗氧化能力(T-AOC)、谷胱甘肽过氧化物酶(GSH-PX)、谷胱甘肽还原酶(GR)的动态变化,为电离辐射防护提供实验依据.方法 对160只仔鼠(出生6～7d)用不同吸收剂量(0Gy、1Gy、3Gy、5Gy、7Gy) X线进行全身辐射,分别于辐射后1d、5d、10d和20d,用比色法检测仔鼠胃组织中T-AOC、GSH-PX、GR酶活性的变化,用显微技术观察仔鼠胃组织结构的变化.结果 1Gy辐射组仔鼠胃T-AOC活性在1～20d时高于对照组,差异显著(P＜0.05),GR活性在1～10d时高于对照组,差异显著(P＜0.05),其他各辐射组T-AOC和GR在辐射后始终低于对照组,差异显著或极显著(P＜0.05或P＜0.01);1Gy辐射组仔鼠胃GSH-PX活性在辐射后1d时低于对照组,差异显著(P＜0.05),以后高于对照组,差异显著(P＜0.05);3Gy辐射组GSH-PX在辐射后1d时高于对照组,差异显著(P＜0.05),以后始终低于对照组,差异显著或极显著(P＜0.05或P＜0.01);其他各辐射组GSH-PX活性始终低于对照组,差异极显著(P＜0.01).随着辐射剂量的增大,实验组仔鼠胃黏膜上皮和腺体均有不同程度的变化,上皮肿胀、空泡化、脱落,胃底腺细胞排列松散、部分降解,胃出血.结论 X线辐射影响仔鼠胃组织结构,这可能与胃抗氧化酶活性降低有关.     

姜黄素对东莨菪碱所致小鼠记忆功能障碍的影响(英文)

目的：探讨中药单体姜黄素对东莨菪碱致小鼠记忆障碍的影响及其可能的机制。方法：用东莨菪碱建立昆明小鼠记忆获得性障碍模型,通过跳台和水迷宫实验观察姜黄素对小鼠学习记忆能力的影响,同时测定其脑组织中乙酰胆碱酯酶、谷胱甘肽过氧化物酶和丙二醛的活性。结果：姜黄素可以减少东莨菪碱所致的记忆获得性障碍小鼠跳台回避反应的错误次数（P<0.05）,延长其逃避潜伏期（P<0.05）,也可以缩短记忆获得障碍小鼠水迷宫中寻找平台的潜伏期（P<0.05）,撤去平台后可以延长小鼠在原平台象限的停留时间（P<0.05）。姜黄素可以降低小鼠脑乙酰胆碱酯酶活性（P<0.01）、提高抗氧化酶谷胱甘肽过氧化物酶活性（P<0.01）、降低脂质过氧化产物丙二醛含量（P<0.01）。结论：姜黄素对记忆获得性障碍有明显的改善作用,其机制可能与影响中枢胆碱能系统、抗氧化损伤有关。     

Urea and sodium: Effect on microsomal ATPase in different parts of the kidney

Summary Microsomal ATPase activity was studied in three regions of the rat kidney: cortex, medulla and papilla. (Na+K)-ATPase activity was highest in the medulla but a substantial activity, comparable to that in the cortex, was also present in the papilla. In the presence of high sodium (200–320 mM) or urea (100–900 mM) progressive inhibition of Mg-ATPase activity was observed in all three regions of the kidney.Urea (900 mM) or Na (320 mM) caused activation of (Na+K)-dependent ATPase in the medulla and inhibition of this enzymatic activity in the papilla of the kidney. Total microsomal ATPase activity in the medulla was unchanged in the presence of urea or sodium but was reduced in the papilla.Urea inhibited non-selectively Mg-p-nitrophenylphosphatase and K-activated p-nitrophenylphosphatase in all three parts of the kidney.These findings may point to a molecular basis for the function of urea and of sodium in the concentrating mechanism of the kidney.This study was supported by the Research Fund of the Israeli Ministry of Health.     

Endrin-induced histopathological changes and lipid peroxidation in livers and kidneys of rats, mice, guinea pigs and hamsters.

Endrin toxicity may be due to an oxidative stress associated with increased lipid peroxidation, decreased glutathione content, and inhibition of glutathione peroxidase activity. Extensive interspecies variability exists in sensitivity towards endrin. Therefore, histopathological changes and lipid peroxidation in the livers and kidneys of rats, mice, hamsters, and guinea pigs were examined 24 hr after the administration of 4 mg endrin/kg body weight orally in corn oil. Degeneration and necrotic changes with inflammatory cell infiltration were observed in livers and kidneys, and interspecies variability occurred. Fatty changes in the form of hepatic foam cells with cytoplasmic vacuolation were present. Lipofuscin pigments, associated with lipid peroxidation, were observed in hepatocytes and Kupffer cells. These histopathological conditions were prevented in rats which had been pretreated with butylated hydroxyanisole, vitamins E and C, or cysteine, antioxidants and free radical scavengers which have previously been shown to inhibit lipid peroxidation. The extent of endrin-induced lipid peroxidation correlated well with the degree of histopathological changes. Thus, histological changes consistent with the induction of an oxidative stress were observed following the administration of endrin to various animal species.     

Reduced serum non-enzymatic antioxidant defense and increased lipid peroxidation in schizophrenic patients on a hypocaloric diet

Introduction

Growing evidence suggests that oxidative stress (OS) may be associated with the pathophysiology underlying schizophrenia (SZ). Some studies indicate that nutritional supplements offer protection from OS, but there is no data about the effect of a hypocaloric diet on OS in this population. Therefore, we aimed to study the effect of a hypocaloric dietary intervention on OS in subjects with SZ.

Methods

A cross-sectional study of 96 participants in outpatient treatment for SZ comprised patients separated into two groups: one group of subjects followed a hypocaloric diet (HD) program (n = 42), while the other group followed a regular diet (RD) with no nutritional restrictions (n = 54). The serum total radical-trapping antioxidant parameter (TRAP), total antioxidant reactivity (TAR) and thiobarbituric acid reactive species (TBARS) levels were assessed.

Results

TRAP levels were lower and TBARS levels were higher in the HD group than in the RD group (p = 0.022 and p = 0.023, respectively). There were no differences in TAR levels between the groups. Additionally, there was a positive correlation between TRAP and TBARS levels after adjusting for BMI and clozapine dose (partial correlation = 0.42, p < 0.001). There were no correlations among the length of illness or diet and the levels of TRAP, TBARS, and TAR.

Conclusions

Subjects with SZ on a hypocaloric diet displayed different OS parameters than those not following a HD. Serum TRAP levels were lower and TBARS levels were higher among SZ subjects with HD compared to SZ subjects without HD. Lower TRAP levels may reflect decreased oxidative stress, whereas higher TBARS levels most likely reflect a biochemical reaction to the decreased TRAP levels. Additionally, TAR levels were similar between groups, suggesting a similar quality of antioxidant defenses, despite quantitative differences between the two dietary protocols in SZ patients under outpatient care.     

Lipid peroxidation,detoxification capacity,and genome damage in mice after transplacental exposure to pharmaceutical drugs

Data on genome damage, lipid peroxidation, and levels of glutathione peroxidase (GPX) in newborns after transplacental exposure to xenobiotics are rare and insufficient for risk assessment. The aim of the current study was to analyze, in an animal model, transplacental genotoxicity, lipid peroxidation, and detoxification disturbances caused by the following drugs commonly prescribed to pregnant women: paracetamol, fluconazole, 5-nitrofurantoin, and sodium valproate. Genome damage in dams and their newborn pups transplacentally exposed to these drugs was investigated using the in vivo micronucleus (MN) assay. The drugs were administered to dams intraperitoneally in three consecutive daily doses between days 12 and 14 of pregnancy. The results were correlated, with detoxification capacity of the newborn pups measured by the levels of GPX in blood and lipid peroxidation in liver measured by malondialdehyde (HPLC-MDA) levels. Sodium valproate and 5-nitrofurantoin significantly increased MN frequency in pregnant dams. A significant increase in the MN frequency of newborn pups was detected for all drugs tested. This paper also provides reference levels of MDA in newborn pups, according to which all drugs tested significantly lowered MDA levels of newborn pups, while blood GPX activity dropped significantly only after exposure to paracetamol. The GPX reduction reflected systemic oxidative stress, which is known to occur with paracetamol treatment. The reduction of MDA in the liver is suggested to be an unspecific metabolic reaction to the drugs that express cytotoxic, in particular hepatotoxic, effects associated with oxidative stress and lipid peroxidation.     

脂质过氧化在肾缺血和缺血再灌注损伤中的变化

本实验观察大鼠肾缺血75min及缺血60min后再灌注15min时肾组织脂质过氧化(LPO)和有关酶类变化。结果显示,肾脏缺血和缺血/再灌注后肾皮质和髓质中脂质过氧化产物丙二醛(MDA)含量均显著增高。超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性无明显变化。缺血/再灌注后黄嘌呤氧化酶(XO)活性显著升高。上述结果提示,肾缺血和缺血/再灌注时的LPO增强与氧自由基(OFR)产生增多有关。但上述二种情况时OFR产生机制不尽相同。     

Influence of serumalbumin and dextran on sodium and water excretion by the isolated dog kidney

Summary The addition of serumalbumin or of dextran reduces sodium and water excretion by isolated kidneys submitted to a saline load. While dextran supplementation produces a considerable drop of glomerular filtration, serumalbumin supplementation induces only slight changes in filtration; a proportional increase of tubular reabsorption is observed. The difference between the response to dextran and serumalbumin may be related to differences in intrarenal blood circulation. Changes in plasma protein concentration play a role in autonomous renal response to saline loading and influence tubular sodium reabsorption. This autonomous renal response is primarily related to plasma dilution.This work has been performed with the help of the Fonds National de la Recherche Scientifique.     

Effect of curcumin on Bcl-2 and Bax expression in nude mice prostate cancer

Prostate cancer is a common malignant tumor in urinary system. Curcumin has curative effect on many kinds of cancers and can inhibit prostate cancer (PC)-3 cells proliferation. This study aimed to explore the curcumin induced prostate cancer cell apoptosis and apoptosis related proteins Bcl-2 and Bax expression. PC-3 cells were injected subcutaneously to the nude mice to establish the tumor model. The nude mice were randomly divided into group C (normal saline), group B (6% polyethylene glycol and 6% anhydrous ethanol), group H, M, L (100 mg/kg, 50 mg/kg, and 25 mg/kg curcumin). The tumor volume was measured every 6 days to draw the tumor growth curve. The mice were killed at the 30^th day after injection to weight the tumor. TUNEL assay was applied to determine cell apoptosis. Immunohistochemistry was used to detect Bcl-2 and Bax expression. The tumor volume and weight in group H, M, L were significantly lower than the control group (C, B) (P<0.05), and the inhibitory rate increased following the curcumin dose increase. Compared with the control group, Bcl-2 expression in group H, M, L gradually decreased, while Bax protein expression increased (P<0.05). The cell apoptosis rate showed no statistical difference between group B and C, while it increased in curcumin group H, M, and L (P<0.05). Curcumin could inhibit PC-3 growth, decrease tumor volume, reduce tumor weight, and induce cell apoptosis under the skin of nude mice by up-regulating Bax and down-regulating Bcl-2.     

麻黄素对小鼠心肌组织结构和总抗氧化能力、过氧化氢酶活力的影响

目的探讨麻黄素对小鼠心肌组织的毒性影响。方法 60只小鼠随机分为麻黄素组和对照组,每组各30只,用递增剂量腹腔连续注射麻黄素溶液(0.0315 g/kg、0.0477 g/kg、0.0564 g/kg)和等量的生理盐水15d(每天两次,每次0.2ml),称量检测小鼠体重和心重的变化,用生物显微技术观察心肌组织结构的变化,用比色法检测血浆肌酸激酶(CK)、肌酸激酶同工酶-MB(CK-MB)和心肌组织总抗氧化能力(T-AOC)、过氧化氢酶(CAT)活力及丙二醛(MDA)含量的变化。结果麻黄素组小鼠体重和心重均低于对照组,小鼠心肌组织出现不同程度的损伤,心肌细胞排列紊乱,闰盘间隙增宽,心肌纤维断裂;麻黄素组小鼠血浆CK、CK-MB活性高于对照组(P0.01),心肌组织T-AOC和CAT的活性降低(P0.05或P0.01),MDA含量则升高(P0.01)。结论麻黄素影响小鼠心肌组织结构,可能与心肌组织抗氧化酶活性降低和丙二醛含量升高有关。     

大鼠自体原位肝移植模型中肠道羟自由基、丙二醛和总抗氧化能力的变化

目的: 建立SD大鼠自体原位肝移植模型,观察自体模拟肝移植后不同时期肠道黏膜病理学变化及肠组织的羟自由基(·OH)、丙二醛(MDA)和总抗氧化能力(T-AOC)的变化。方法: SD大鼠36只,随机分为假手术组(S组)和模型组(M组),模型组根据肝脏再灌注时间,再分为再灌注2 h模型组(M1组)、再灌注4 h模型组(M2组)、再灌注8 h模型组(M3组)、再灌注16 h模型组(M4组)和再灌注24 h模型组(M5组)5个亚组。对照组在麻醉后只进行开腹和血管的分离,不进行肝脏的阻断和灌注;模型组则进行自体肝移植手术。分别在肝脏再灌注后2、4、8、16、24 h取肠组织,观察其病理形态学变化及·OH、MDA和T-AOC的变化。结果: (1)与S组相比,M组大鼠肠黏膜在肝脏再灌注后出现明显的病理学损伤,可见上皮下间隙的扩大,甚至出现绒毛上皮和固有层分离,再灌注8 h时最为显著,再灌注24 h开始修复;(2)与S组相比,M2、M3和M4组·OH水平明显升高(P<0.05),M1、M2、M3组MDA含量明显升高(P<0.05),M1、M2、M3和M4组T-AOC明显降低(P<0.05)。结论: 自体原位肝移植可使大鼠肠黏膜·OH和MDA含量增加,T-AOC下降,肠道出现可逆性病理损伤。     

Activity of antioxidant enzymes and lipid peroxidation in intact and mutagen-treated NZW mice

Catalase and superoxide dismutase activities in the liver of NZW mice are 29.3 μmol H₂O₂/min×mg protein and 10.6 U/mg protein, respectively. The rate of accumulation of lipid peroxidation (LPO) products is low within the first 60 min of incubation of liver homogenates with ascorbate and then rapidly increases. A similar process is observed with Fe+ascorbate system, where LPO rate is markedly higher and lag-period lasts 10 min. Under the action of cyclophosphane the activity of catalase increases by 32%, while that of superoxide dismutase decreases by 46%, which is accompanied by a decline in the sensitivity of liver tissue to LPO induction. When LPO is inducedin vitro by ascorbate, lag-period decreases 2-fold, while the rate of accumulation of LPO products increases by 38% and their maximum level by 35% compared with the control. Similar processes develop in the Fe+ascorbate system. Dioxydine induces no significant changes in the activities of catalase and superoxide dismutase as well as in LPO product accumulation in the ascorbate and Fe+ascorbate systems. Translated fromByulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 123, No. 4, pp. 381–384, April, 1997     

Age-related changes in antioxidant enzymes and lipid peroxidation in brains of control and transgenic mice overexpressing copper-zinc superoxide dismutase

The aim of our study was first to obtain a comprehensive profile of the brain antioxidant defense potential and peroxidative damage during aging. We investigated copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), seleno-dependent glutathione peroxidase (GSH-PX), glutathione reductase (GSSG-R) activities, endogenous and in vitro stimulated lipid perxidation in 40 brains of control mice divided into 3 age groups: 2 months (young), 12 months (middle-aged) and 28 months (old). We found a positive correlation between age and activities of CuZnSOD (r = 0.47); P < 0.01) and GSH-PX (r = 0.72; P < 0.0001). CuZnSOD and GSH-PX activities are independently regulated during brain aging since temporal changes of these two enzymes do not correlate. No modification in MnSOD activity and basal lipid peroxidation was observed as a function of age. Nevertheless, stimulated lipid peroxidation was significantly higher at 12 months (6.53 ± 0.71 μmole MDA/g tissue) thatn at 2 months (5.69 ± 0.90) and significantly lower than 28 months (5.13 ± 0.33) than at 12 months.Second, we used genetic manipulations to construct transgenic mice that specifically overexpress CuZnSOD to understand the role of CuZnSOD in neuronal aging. The human CuZnSOD transgene expression was stable during aging. The increased CuZnSOD activity in the brain (1.9-fold) of transgenic mice resulted in an enhanced rate of basal lipid peroxidation and in increased MnSOD activity in the 3 age groups. Other antioxidant enzymes did not exhibit modifications indicating the independence of the regulation between CuZnSOD and glutathione-related enzymes probably due to their different cellular localization in the brain.     

Determination of serum and organ malondialdehyde (MDA) concentration, a lipid peroxidation index, in Trypanosoma brucei-infected rats

Lipid peroxidation was assessed in the sera and various organs of rats experimentally infected with Trypanosoma brucei. Thirty-six adult albino rats divided into 2 groups of eighteen rats each were used in this study. In experiment one, a group of 18 rats were used and they were divided into three groups (A, B and C) of six rats each. Groups B and C rats were infected with 1.54 × 10⁵ trypanosomes per rat intraperitoneally, whereas group A served as uninfected control. The rats were bled on day 0 and subsequently at 7-day intervals for packed cell volume (PCV), sera peroxidation index and parasitaemia. Also, temperature and weight were taken on day 0 and subsequently at 7-day intervals. In experiment 2, 18 rats were also used. Six rats each were sacrificed on days 0, 14 and 28-postinfection. Five rats each were sacrificed on day 14 and day 28 post-infection (PI) from group B, and their organs were promptly collected and washed with normal saline and used for organ malondialdehyde (MDA) concentration. The infection led to an increase in lipid peroxidation index (MDA concentration) of sera samples. The serum MDA concentration of the infected rat group was significantly (p < 0.01) higher than in the uninfected group on days 21 and 28 PI. The increase was however reversed by diminazene aceturate (Berenil; Hoechst, Ireland) treatment at the dosage of 7 mg/kg body weight administered on day 14 PI. The organ lipid peroxidation index also increased significantly (p < 0.05) in the eye, lung and spleen. However, there was no significant (p > 0.05) increase of lipid peroxidation index in the kidney, heart, liver, testes and brain. Also, the mean weekly MDA concentration increased as the disease progressed, the mean weekly temperature and parasitaemia also increased, but the reverse was the case with the mean weekly body weight and PCV which declined as the disease progressed. The findings are indication that oxidative stress plays an important role in the pathology of trypanosomosis.     

母鼠注射麻黄素对仔鼠肝组织结构和总抗氧化能力、谷胱甘肽转移酶活性及丙二醛含量的影响

目的:探讨妊娠或哺乳期女性食用麻黄素对胎幼儿的影响。方法:给妊娠和哺乳期母鼠连续腹腔注射不同剂量(2、4、6 g/L)的麻黄素溶液,用分光光度法检测仔鼠肝组织总抗氧化能力(T-AOC)、谷胱甘肽转移酶(GST)活性及丙二醛(MDA)含量的变化,生物显微技术观察仔鼠肝组织结构的变化。结果:麻黄素组仔鼠肝组织结构出现不同程度的病理性变化,肝血窦扩张,并有内皮细胞脱落、肝板萎缩等现象,仔鼠肝组织T-AOC、GST活性降低,肝组织MDA含量升高,与对照组比较差异有统计学意义。结论:母鼠注射麻黄素会影响仔鼠肝组织结构和功能,麻黄素及其代谢物可能经胎盘或乳汁进入仔鼠体内损伤仔鼠肝组织的抗氧化系统,机体脂质过氧化反应增强,影响细胞的能量代谢。     

Effect of raising the transtubular oncotic gradient on sodium excretion in the dog

Summary In dogs treated with high doses of aldosterone and pitressin, sodium excretion is reduced following the rise in the transtubular oncotic pressure gradient induced either by systemic injections of albumin or dextran or by systemic infusion of small amounts of adrenalin. This effect is obtained under conditions of a constant filtered sodium load. The increased tubular sodium reabsorption is not accompanied by any change in renal oxygen consumption and is independent of plasma volume changes. These results demonstrate that a small fraction of filtered sodium is reabsorbed by a process governed by the transtubular oncotic pressure gradient.     

Relationship between the clinical scoring and demyelination in central nervous system with total antioxidant capacity of plasma during experimental autoimmune encephalomyelitis development in mice

Experimental autoimmune encephalomyelitis (EAE) was induced in a mouse model (C57/BL6) to investigate the antioxidant status of animals at various clinical stages of the disease. For this purpose, blood, brain and spinal cord samples from EAE mice were collected and examined at different scores following post-immunization with myelin oligodendrocyte glycoprotein (MOG). The clinical sign of mobility of animals on different days was associated with gradual increase in lipid peroxidation products (malondialdehyde, i.e. MDA) in brain and spinal cord. Changes in lipid peroxidation during EAE progression was inversely related to superoxide dismutase (SOD) activity in erythrocyte preparation. However, suppression of catalase in erythrocytes, tissue glutathione (GSH) and plasma total antioxidant capacity (FRAP assay) were the early events in EAE, occurred during scores 1 and 2. Biochemical alterations were corroborated with histopathological observations showing demyelination and inflammatory foci in central nervous system (CNS) of animals suffering from partial hind limb paralysis (score 3). These data suggest that generation of MDA in CNS is a continuous process during EAE induction and suppression of antioxidant factors are early events of the disease, but crucial in increasing the vulnerability of CNS to demyelinating lesions.     

Effects of indomethacin on renal hemodynamics and on water and sodium excretion by the isolated dog kidney

Summary Blood-perfused isolated dog kidneys demonstrate steady increases in blood flow and in water and sodium excretion which could be attributed to the accumulation of renal prostaglandins in the perfusing blood. This hypothesis was tested by adding indomethacin, a potent inhibitor of prostaglandins synthesis, to the perfusing blood.Indomethacin completely prevented the vasodilation observed in control kidneys, without affecting glomerular filtration rate. Urine volume was not modified but sodium excretion was enhanced while the steady free water clearance increment observed in the control kidneys was depressed by indomethacin. The sum of sodium and free water clearances which, in the absence of antidiuretic hormone, constitutes an index of the part of the filtered load of solutes which escapes proximal tubular reabsorption, was not modified by indomethacin. Finally, indomethacin partially maintained the osmotic cortico-papillary gradient which was abolished after 2 hrs perfusion in control kidneys.These data suggest that prostaglandins accumulation in the blood is probably the major cause of the vasodilation taking place in isolated blood-perfused kidneys. This vasodilation does not account for decreased proximal reabsorption but partially explains the ADH-resistant diabetes insipidus developing in the isolated kidney. Moreover, indomethacin inhibits sodium reabsorption in the ascending limb of Henle's loop and increases water transport in the collecting duct.     

Changes in the serum antioxidant system and lipid peroxidation under the influence of asbestos

The iron content, the state of the serum antioxidant system, and their relationship with the changes in lipid peroxidation in rat liver and lungs at the early stages of chrysotile-asbestos action, and the effect of the naturally occurring flavonoid rutin are studied. Intensification of lipid peroxidation in the liver and lungs and an increase in the oxyproline content, which correlates with the rise in serum antioxidant activity, are observed four weeks after a single intratracheal administration of 50 mg asbestos. The total serum iron content remains unchanged. Rutin has a pronounced anti-asbestos effect, inhibits the early stages of fibrosis, and facilitates normalization of the antioxidant system imbalance induced by asbestos. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 118, N ^o 8 pp. 145–147, August, 1994