Protective Effects of Melatonin Against Formaldehyde-Induced Oxidative Damage and Apoptosis in Rat Testes: An Immunohistochemical and Biochemical Study

This study investigated the protective effects of melatonin against formaldehyde-induced oxidative damage and apoptosis in rat testes. A total of 21 male Wistar rats were divided into three groups. Group I was used as a control, Group II was injected every other day with formaldehyde for 1 month, whereas Group III was injected every other day with formaldehyde and melatonin for 1 month. At the end of the experimental period animals were sacrificed and the testes removed and dissected from the surrounding tissues for immunohistochemical evaluation. In addition, the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) were determined. The levels of SOD and GSH-Px decreased significantly, whereas the level of MDA significantly increased in animals treated with formaldehyde compared with the controls. Apoptosis of spermatogenetic and Leydig cells of testicular tissues was observed. In contrast, rats with melatonin SOD and GSH-Px enzyme activity increased whereas MDA levels decreased with formaldehyde exposure along with apoptosis. In view of the present findings, it is suggested that melatonin treatment may prevent formaldehyde-induced oxidative damage and apoptosis in rat testes.     

Protective effect of melatonin against formaldehyde-induced kidney damage in rats

This study was undertaken to investigate the protective effects of melatonin against formaldehyde-induced renal damage in rats. For this purpose, 21 male Wistar rats were divided into three groups. The animals in Group I were used as a control, whereas the rats in group II were injected every other day with formaldehyde. The rats in group III received melatonin daily while exposed to formaldehyde. At the end of the 14-day experimental period, all rats were killed by decapitation, and the kidneys were removed. Some of the renal tissue specimens were used for determination of superoxide dismutase, glutatione peroxidase enzyme activities, and malondialdehyde levels. The remaining kidney tissue specimens were used for light microscopic evaluation. The renal tissue activities of superoxide dismutase and glutatione peroxidase were significantly decreased, and malondialdehyde levels were significantly increased in rats treated with formaldehyde compared with those of the control animals. In the light microscopic evaluation of this group, degenerative glomerules, vacuolization and dilatation of distal tubules, and vascular congestion were detected. However, an increase was observed in activities of superoxide dismutase and glutatione peroxidase enzymes, and a decrease of malondialdehyde levels in animals treated with formaldehyde plus melatonin was observed. Furthermore, the histopathological changes caused by formaldehyde were disappeared except for minimal tubular dilatation in this group. In conclusion, the biochemical and histological findings of our study suggest that melatonin administration prevents formaldehyde-induced oxidative renal damage in rats.     

Melatonin protects rat liver against irradiation-induced oxidative injury

The aim of this study was to investigate the antioxidant roles of different doses of melatonin (5 and 10 mg x kg (-1) ) against gamma-irradiation-caused oxidative damage in liver tissue after total body irradiation (TBI) with a single dose of 6.0 Gy. Fifty adult rats were divided into 5 equal groups, 10 rats each. Groups I and II were injected with 5 and 10 mg x kg (-1) of melatonin, and group III was injected with an isotonic NaCl solution. Group IV was injected with only 5 mg x kg (-1) of melatonin. Group V was reserved as a sham control. Following a 30-min-period, 6.0 Gy TBI was given to groups 1, 2 and 3 in a single fraction. The liver malondialdehyde (MDA) levels, super oxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were measured in all groups. TBI resulted in a significant increase in the liver tissue MDA levels and a decrease of SOD and GSH-Px activities. The results demonstrated that the liver tissue MDA levels in irradiated rats that were pretreated with melatonin (5 or 10 mg x kg (-1) ) were significantly decreased, while the SOD and GSH-Px activities were significantly increased. Decreasing the MDA levels by melatonin was dose dependent, but the liver tissue SOD and GSH activities were not. The data obtained in this study suggest that melatonin administration prior to irradiation may prevent liver damage by irradiation.     

Protective effects of omega-3 essential fatty acids against formaldehyde-induced cerebellar damage in rats

This study aimed to investigate changes in the cerebellum of formaldehyde-exposed rats and the effects of omega-3 fatty acids on these changes. The study involved 21 male Wistar-Albino rats which were divided into three groups. The rats in Group I comprised the control group. The rats in Group II were injected with intraperitoneal 10% formaldehyde every other day. The rats in Group III received omega-3 fatty acids daily while exposed to formaldehyde. At the end of the 14-day experimental period, all rats were killed by decapitation and the cerebellum removed. The activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), xanthine oxidase (XO), and malondialdehyde (MDA) levels were determined in cerebellum specimens by using spectrophotometric methods. In our study, levels of SOD and CAT were significantly decreased, and GSH-Px, XO, MDA levels were significantly increased in rats treated with formaldehyde compared with those of the controls. Whereas, it was seen that there was an increase in SOD and CAT enzyme activities and decrease in MDA, XO, and GSH-Px levels in rats administered to omega-3 fatty acids with exposure of formaldehyde. It was determined that exposure of formaldehyde increased free radicals in cerebellum of rats and this increase was prevented by administration of omega-3 fatty acids.     

Effects of omega-3 essential fatty acids against formaldehyde-induced nephropathy in rats

The aim of this study was to examine the toxicity of formaldehyde (FA) on the kidney and the protective effects of omega-3 essential fatty acids against these toxic effects. Twenty-one male Wistar rats were divided into three groups. Rats in Group I comprised the controls, while the rats in Group II were injected every other day with FA. Rats in Group III received omega-3 fatty acids daily while exposed to FA. At the end of the 14-day experimental period, all rats were killed by decapitation and the kidneys removed. Some of the kidney tissue specimens were used for determination of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities, and malondialdehyde (MDA) levels. The remaining kidney tissue specimens were used for light microscopic evaluation. The levels of SOD and GSH-Px were significantly decreased, and MDA levels were significantly increased in rats treated with FA compared with those of the controls. Furthermore, in the microscopic examination of this group, glomerular and tubular degeneration, vascular congestion and tubular dilatation were observed. However, increased SOD and GSH-Px enzyme activities, and decreased MDA levels were detected in the rats administered omega-3 fatty acids while exposed to FA. Additionally, kidney damage caused by FA was decreased and structural appearance was similar to that of the control rats in this group. In conclusion, it was determined that FA-induced kidney damage was prevented by administration of omega-3 essential fatty acids.     

姜黄素对甲醛致A549细胞氧化损伤拮抗作用

目的探讨姜黄素对甲醛致细胞氧化损伤的拮抗效应。方法采用A549细胞株作为实验材料,实验设对照组、0.1 mmol/L甲醛染毒组,姜黄素组(0.1 mmol/L甲醛+2.5～20.0 mg/L姜黄素),检测A549细胞中一氧化氮合酶(NOS),丙二醛(MDA),超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH-Px)活性。结果甲醛染毒组A549细胞SOD、NOS和GSH-Px活性分别为(21.79±1.13)、(1.88±0.16)与(27.83±0.2)U/mgprot,与对照组比较,SOD、NOS和GSH-Px活性明显下降(P<0.05),MDA含量[(3.87±0.153.87)nmol/mgprot]明显升高(P<0.05)。与甲醛染毒组比较,各姜黄素组GSH-Px活性上升、MDA含量下降(P<0.05),与对照组比较,40 mg/L姜黄素组GSH-Px活性、MDA含量差异无统计学意义(P>0.05)。结论姜黄素可提高A549细胞抗氧化酶活性,并存在剂量效应关系。     

牛磺酸对甲基汞致大鼠脑氧化损伤的保护作用

[目的]探讨甲基汞致大鼠脑氧化损伤及牛磺酸对氧化损伤的保护作用。[方法]将24只健康清洁级Wistar大鼠按体质量随机分为4组,每组6只,分别为对照组、低剂量染汞组、高剂量染汞组和牛磺酸干预组。周一至周五每天进行染毒,对照组腹腔注射生理盐水,低剂量染汞组腹腔注射4μmol/kg氯化甲基汞,高剂量染汞组和牛磺酸干预组腹腔注射12μmol/kg氯化甲基汞;每周一、三、五染毒前2h进行预处理,对照组、低剂量染汞组和高剂量染汞组皮下注射生理盐水,牛磺酸干预组皮下注射1mmol/kg的牛磺酸;连续进行4周,最后一次染毒后,处死大鼠。取大脑皮质测定：活性氧（ROS）、巯基、羰基、丙二醛（MDA）的含量,超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-px）的活性及细胞凋亡率。[结果]与对照组比较,低、高汞组大鼠的体质量增长幅度降低（P〈0.05,P〈0.01）;ROS分别是其1.8和3.9倍（均P〈0.01）;SOD和GSH-px的活性均降低;巯基的含量降低;羰基的含量升高;MDA增加;细胞凋亡率分别升高3.4和10.0倍。牛磺酸干预组与高剂量染汞组比较,ROS的生成量降低了17%;SOD、GSH-px的活性有不同程度的升高;巯基、羰基和MDA的含量也有不同程度的改变;细胞凋亡率为高汞组的44%。[结论]甲基汞可导致脑氧化损伤,牛磺酸对甲基汞所致氧化损伤具有一定的保护作用。     

Effects of xylene and formaldehyde inhalations on renal oxidative stress and some serum biochemical parameters in rats

In this study, it was aimed to demonstrate the possible renal oxidative stress and some serum biochemical parameters and their alterations caused by the exposure to xylene and formaldehyde (HCHO) in rats. Weighing 150-200g, 12-week-old, 24 female Sprague-Dawley rats were used. The rats were randomly divided into four groups: Group 1 (control), Group 2 (300-ppm technical xylene), Group 3 (6-ppm HCHO) and Group 4 (150-ppm technical xylene + 3-ppm HCHO). The animals were exposed to gases eight hours per day for six weeks. Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities, glutathione (GSH) and malondialdehyde (MDA) levels were measured. In addition, serum total protein, albumin, urea and creatinine levels were evaluated. Compared with the control animals, urea levels increased significantly in all groups (P < 0.001). GSH activities and MDA levels increased in xylene and xylene + HCHO groups (P < 0.05). No statistically considerable differences were found in SOD, CAT and GSH-Px activities, total protein, albumin and creatinine levels among all groups (P > 0.05). The present study indicates but not statistically confirms the renal toxicity of the exposures to xylene, HCHO and a mixture of them.     

褪黑素对溴氰菊酯致大鼠脑组织氧化损伤的保护作用

目的探讨褪黑素(melatonin,MT)对溴氰菊酯(deltamethrin,DM)诱发大鼠大脑皮层、海马、小脑组织氧化性损伤的保护作用。方法35只Wistar雄性大鼠按体重随机分为5组:橄榄油对照组(1 ml/kg橄榄油)、MT对照组(25.0 mg/kg MT)、DM组(12.5 mg/kg DM)、MT1组(25.0 mg/kg MT 12.5 mg/kg DM)、MT2组(2.5 mg/kg MT 12.5 mg/kg DM)。每组7只,每组连续5 d腹腔注射相应剂量药物。第5天给药后4 h,每组大鼠分别断头处死,Spectramx M2多模式全能酶标仪比色测定大鼠大脑皮层、海马、小脑组织匀浆上清中丙二醛(MDA)、谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)活力。结果与橄榄油对照组相比,DM组大脑皮层、海马、小脑组织MDA含量分别上升28.10%、39.25%、56.39%,差异有统计学意义(P<0.05),大脑皮层、海马组织GSH-Px活力分别下降24.08%、45.01%,小脑组织CAT活力降低27.83%,差异有统计学意义(P<0.05)。与DM组相比,MT1组大脑皮层、海马、小脑组织的MDA含量分别下降31.12%、41.49%、32.69%,差异有统计学意义(P<0.05);MT1组大脑皮层的GSH含量、CAT、GSH-Px活力分别升高了48.33%、36.11%、56.59%,MT1组海马组织的GSH含量、CAT、GSH-Px活力分别升高了64.51%、30.32%、79.35%,差异均有统计学意义(P<0.05);MT2组大脑皮层、海马MDA含量分别下降了22.96%、25.00%,MT2组海马组织的GSH-Px活力升高了123.33%,差异有统计学意义(P<0.05)。结论DM能诱发大鼠脑组织的氧化损伤,MT对DM引起的大鼠脑组织的氧化损伤有预防作用。     

Radioprotective effects of melatonin on radiation-induced cataract

One of the mechanisms proposed to explain lens opacification is the oxidation of crystallins, either by radiation or reactive oxygen species (ROS). It has been shown that melatonin has both an anti-peroxidative effect on several tissues and a scavenger effect on ROS. The purpose of this study was to determine the antioxidant role of melatonin (5 mg/kg/day) against radiation-induced cataract in the lens after total-cranium irradiation of rats with a single dose of 5 Gy. Sprague-Dawley rats were divided into four groups. Control group received neither melatonin nor irradiation. Irradiated rats (IR) and melatonin+irradiated rats (IR+Mel) groups were exposed to total cranium irradiation of 5 Gy in a single dose by using a cobalt-60 teletherapy unit. IR+Mel and melatonin (Mel) groups were administered 5 mg/kg melatonin daily by intraperitoneal injections during ten days. Chylack's cataract classification was used in this study. At the end of the 10th day, the rats were killed and their eyes were enucleated to measure the antioxidant enzymes i.e. the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and lipid peroxidation level (malondialdehyde (MDA)). Irradiation significantly increased the MDA level, as an end product of lipid peroxidation, and also significantly decreased SOD and GSH-Px activity, emphasizing the generation of increased oxidative stress. Rats injected with melatonin only did not cause cataract formation. Melatonin supplementation with irradiation significantly increased the activity of SOD and GSH-Px enzymes and significantly decreased the MDA level. Total cranium irradiation of 5 Gy in a single dose enhanced cataract formation, and melatonin supplementation protected the lenses from radiation-induced cataract formation. Our results suggest that supplementing cancer patients with adjuvant therapy of melatonin may reduce patients suffering from toxic therapeutic regimens such as chemotherapy and/or radiotherapy and may provide an alleviation of the symptoms due to radiation-induced organ injuries.     

银杏叶提取物对酒精所致大鼠睾丸氧化损伤的保护作用的研究

目的研究银杏叶提取物(EGB)对酒精所致大鼠睾丸氧化损伤的预防保护作用。方法雄性SD大鼠30%酒精灌胃(2.37g/kgbw)前,EGB采用分组(低剂量组48μg/gbw和高剂量组96μg/gbw)预防性给药的方法。于实验90d检测大鼠睾丸组织中超氧化物歧化酶(SOD)、谷胱甘肽转移酶(GST)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、和谷胱甘肽(GSH)、活性氧(ROS)以及丙二醛(MDA)的含量。通过亚细胞分离方法提取大鼠睾丸微粒体,测定微粒体血红素氧化酶-1(HO-1)活性。采用RT-PCR检测睾丸组织中血红素氧化酶-1(HO-1)mRNA表达水平。结果慢性酒精摄入90d后,EGB组睾丸匀浆ROS、MDA较酒精组有明显降低(P<0.05);相反,GST、G-Px、CAT、SOD、HO-1活性以及GSH均有显著性升高(P<0.05);EGB诱导HO-1高表达。结论长期慢性酒精摄入引起大鼠睾丸氧化损伤。EGB可作为一种预防性的抗氧化剂减轻这种氧化损伤;其机制可能与诱导HO-1高表达,清除自由基,抑制脂质过氧化反应有关。     

Active smoking causes oxidative stress and decreases blood melatonin levels

Oxidative effects via free radical generation in smokers have been widely investigated. They cause lipid peroxidation, oxidation of proteins and damage to mainly lung and other tissues. In humans, antioxidative capacity of serum is related to antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and melatonin. The effect of cigarette smoking on plasma levels of melatonin and antioxidant enzymes has not been established together yet. Also, it may not be clear if melatonin levels are affected by smoking and melatonin has a protective effect on cigarette smoking-induced free radical damage. The aim of this study is to investigate the relationship between smoking and antioxidant capacity including melatonin, a powerful endogenous antioxidant, and antioxidant enzymes in teenage girls who are active smokers. Additionally, malondialdehyde (MDA) levels were determined in those who have smoked at least one packet a day for three or more years. MDA levels have been used as a convenient index of the lipid peroxidation-related oxidative damage of tissues. Twenty-one young female active smokers who study at the School of Nursing and 21 nonsmoking students (as controls) at the same school were included in the study. The activities of two principal antioxidant enzymes SOD, GSH-Px and plasma levels of MDA were significantly increased but melatonin content of the blood was significantly decreased as compared to nonsmokers. In spite of an increase in antioxidant enzyme activities, MDA levels were slightly increased in smokers. This indicates that antioxidant self-defence mechanisms may not sufficiently protect the respiratory system from smoke-mediated oxidative injury. This result may be related to low melatonin levels in teenage female smokers. It seems that melatonin can reduce free radical damage to the respiratory system induced by cigarette smoke. Further experimental investigations with exogenous melatonin treatments will be needed.     

番茄红素抗氧化损伤的实验研究

目的观察番茄红素对臭氧所致大鼠氧化损伤的保护作用。方法利用大鼠吸入臭氧制造损伤模型,同时灌胃番茄红素,6周后检测大鼠血清及肝脏中的超氧化物歧化酶(SOD)活性、谷胱甘肽过氧化物酶(GSH-Px)活力及丙二醛(MDA)含量。结果高、低剂量组与损伤模型组相比,SOD和GSH-Px活力升高,MDA含量下降,差异显著(P<0.05)。结论番茄红素对臭氧所致大鼠氧化损伤具有一定的保护作用。     

纳米硫化铅对大鼠海马及皮质氧化损伤作用的研究

目的探讨纳米硫化铅对大鼠海马及皮质的氧化损伤作用。方法清洁级SD雄性大鼠60只,随机分为3组,即对照组、纳米硫化铅低、高剂量组,低、高剂量组分别气管灌注15、30mg/kg粒径20nm的硫化铅混悬液1ml,每周1次,连续染毒3个月后测定3个组大鼠体质量变化;检测大鼠血清、海马及皮质中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力和丙二醛(MDA)含量。结果染毒组大鼠血清、海马及皮质中SOD、GSH-Px的活力及MDA含量分别与对照组比较,差异均有统计学意义(P<0.05)。染毒组大鼠血清、海马及皮质中SOD、GSH-Px活力均降低,MDA含量增高。结论纳米硫化铅可能引起海马及皮质中SOD、GSH-Px活力降低,MDA含量增加,可导致海马及皮质抗氧化能力减弱。     

900 MHz radiofrequency-induced histopathologic changes and oxidative stress in rat endometrium: protection by vitamins E and C

There are numerous reports on the effects of electromagnetic radiation (EMR) in various cellular systems. Mechanisms of adverse effects of EMR indicate that reactive oxygen species (ROS) may play a role in the biological effects of this radiation. The aims of this study were to examine 900 MHz mobile phone-induced oxidative stress that promotes production of ROS and to investigate the role of vitamins E and C, which have antioxidant properties, on endometrial tissue against possible 900 MHz mobile phone-induced endometrial impairment in rats. The animals were randomly grouped (eight each) as follows: 1) Control group (without stress and EMR, Group I), 2) sham-operated rats stayed without exposure to EMR (exposure device off, Group II), 3) rats exposed to 900 MHz EMR (EMR group, Group III) and 4) a 900 MHz EMR exposed + vitamin-treated group (EMR + Vit group, Group IV). A 900 MHz EMR was applied to EMR and EMR + Vit group 30 min/day, for 30 days using an experimental exposure device. Endometrial levels of nitric oxide (NO, an oxidant product) and malondialdehyde (MDA, an index of lipid peroxidation), increased in EMR exposed rats while the combined vitamins E and C caused a significant reduction in the levels of NO and MDA. Likewise, endometrial superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities decreased in EMR exposed animals while vitamins E and C caused a significant increase in the activities of these antioxidant enzymes. In the EMR group histopathologic changes in endometrium, diffuse and severe apoptosis was present in the endometrial surface epithelial and glandular cells and the stromal cells. Diffuse eosinophilic leucocyte and lymphocyte infiltration were observed in the endometrial stroma whereas the combination of vitamins E and C caused a significant decrease in these effects of EMR. It is concluded that oxidative endometrial damage plays an important role in the 900 MHz mobile phone-induced endometrial impairment and the modulation of oxidative stress with vitamins E and C reduces the 900 MHz mobile phone-induced endometrial damage both at biochemical and histological levels.     

Hepatotoxic activity of toluene inhalation and protective role of melatonin

This study was designed to investigate the harmful effects of toluene inhalation in the liver of rats and possible protective effects of melatonin on these detrimental effects. For this purpose, 21 adult male Wistar-albino rats were randomly divided into three equal groups. Animals in group I were used as control. The rats in group II were exposed to toluene (3000 ppm/1 hour/day) for 4 weeks, while the rats in group III were treated with melatonin (10 mg/kg/day, intraperitoneally [ip]) plus toluene inhalation. At the end of the experimental period, liver and blood samples were taken from the decapitated animals. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin and albumin levels were determined. Liver tissue sections were stained with routine histological methods and examined under the light microscope. In addition, the sections were immunohistochemically stained using avidin-biotin-peroxidase method for determination of apoptosis. The liver tissue activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and malondialdehyde (MDA) levels were also measured. Toluene inhalation significantly increased serum ALT, AST and tissue MDA, and decreased serum albumin, but did not affect serum ALP, total bilirubin levels and tissue SOD, GSH-Px and CAT activity when compared with controls. The increases in tissue MDA and serum ALT and AST levels induced by toluene inhalation were significantly inhibited by melatonin treatment. In light microscopic observations of tissues from toluene-inhaled rats, massive hepatocyte degeneration, ballooning degeneration and mild pericentral fibrosis were observed. Bax immune reactivity was also increased significantly. Melatonin treatment decreased the balloon degeneration, fibrosis and Bax immune reactivity in the liver of toluene-inhaled rats. In view of the present findings, it is suggested that melatonin has hepatoprotective effects against toluene toxicity via primarily antioxidative properties.     

硒多糖对镉中毒大鼠肾保护作用的研究

目的 探讨硒多糖对镉中毒大鼠肾的保护作用。方法 经腹腔注射2．5mg／kg．d氯化镉，连续3d，诱发大鼠肾中毒，同时给大鼠饮用不同剂量的硒多糖水溶液30d，分别测定肾组织匀浆的SOD、GSH-Px的活性，MDA含量，并同时观察大鼠肾组织的形态。结果 硒多糖能明显提升SOD、GSH-Px的括性，显著降低MDA含量，使大鼠肾脏维持正常的生理功能及组织结构。结论 硒多糖对镉中毒大鼠肾损伤有一定的保护作用。     

番茄红素对大鼠肺氧化损伤的影响

目的　观察臭氧对大鼠造成的氧化损伤和番茄红素 (LP)对损伤的影响。方法　利用臭氧吸入造成氧化损伤模型 ,以黄嘌呤氧化酶法测定血清和肺匀浆的SOD活性 ,硫代巴比妥显色法测定MDA含量 ,DTNB比色法测定GSH Px活力。结果　各番茄红素给药组的大鼠血清和肺组织的SOD活性、GSH Px活力上升 ,MDA含量降低 ,与模型组相比差异有显著性 (P <0 0 5 )。结论　番茄红素可以保护臭氧造成的大鼠氧化损伤     

Inhibitory effect of melatonin on products of lipid peroxidation resulting from chronic ethanol administration

Despite decades of research, the role of free radicals in alcohol-induced organ injury is still a matter of debate. The present work was designed to investigate the potential protective effect of melatonin, a reported radical scavenger and antioxidant, on free radical toxicity induced by chronic ethanol administration. The major end-point of oxidative damage measured in this report was lipid peroxidation. Four groups of male Sprague-Dawley rats were used. The first group served as untreated controls and received a daily injection of alcoholic (<1% ethanol) saline. The second group of rats received daily at 18:00 a single subcutaneous injection of melatonin (10 mg/kg). Group 3 rats received only ethanol (3 g/kg) for 30 consecutive days; the ethanol was given at 18:30. The final group of rats was given both melatonin and ethanol with melatonin preceding ethanol by 30 min. Products of lipid peroxidation [malondialdehyde (MDA) and 4-hydroxyalkenals (4-HDA)] were measured in the brain, heart, liver, lung and testes. At the conclusion of the study, MDA + 4-HDA levels were significantly increased in brains, hearts, lungs and testes, but not livers, of alcohol-treated compared with control rats. The percentage increases in lipid peroxidation products were 21.8%, 28.8%, 35.9% and 45.3% for brain, heart, lung and testes, respectively. In animals given melatonin 30 min before ethanol, the increases in MDA + 4-HDA levels were significantly reduced in all organs investigated, with levels not different from those in control rats. Based on these findings, it is speculated that melatonin's direct and indirect antioxidative actions inhibited alcohol-induced lipid peroxidation. These results suggest a new strategy for the treatment of alcohol-related diseases using melatonin as an antioxidant to reduce the damage inflicted by aggressive radical species.     

有机磷农药中毒对小鼠脑损伤的实验研究

目的 探讨有机磷农药对正常小鼠脑部损伤的程度。方法 用灌胃法对小鼠进行急性染毒后，测定小鼠脑胆碱脂酶活性(ChE)、脑脂质过氧化产物丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性、谷胱廿肽过氧化物酶(GSH-Px)活性。结果 测定组与对照组比较，小鼠脑胆碱脂酶活性明显降低，而脑MDA、SOD、GSH-Px活性无明显改变。结论 经有机磷农药急性染毒后的小鼠脑ChE活性降低，脑MDA、SOD、GSH-Px活性无明显改变。