A novel antioxidant agent caffeic acid phenethyl ester prevents long-term mobile phone exposure-induced renal impairment in rat

Caffeic acid phenethyl ester (CAPE), a flavonoid like compound, is one of the major components of honeybee propolis. It has been used in folk medicine for many years in Middle East countries. It was found to be a potent free radical scavenger and antioxidant recently. The aim of this study was to examine long-term applied 900 MHz emitting mobile phone-induced oxidative stress that promotes production of reactive oxygen species (ROS) and, was to investigate the role of CAPE on kidney tissue against the possible electromagnetic radiation (EMR)-induced renal impairment in rats. In particular, the ROS such as superoxide and nitric oxide (NO) may contribute to the pathophysiology of EMR-induced renal impairment. Malondialdehyde (MDA, an index of lipid peroxidation) levels, urinary N-acetyl-β-d-glucosaminidase (NAG, a marker of renal tubular injury) and nitric oxide (NO, an oxidant product) levels were used as markers of oxidative stress-induced renal impairment and the success of CAPE treatment. The activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in renal tissue were determined to evaluate the changes of antioxidant status. The rats used in the study were randomly grouped (10 each) as follows: i) Control group (without stress and EMR), ii) Sham-operated rats stayed without exposure to EMR (exposure device off), iii) Rats exposed to 900 MHz EMR (EMR group), and iv) A 900 MHz EMR exposed + CAPE treated group (EMR + CAPE group). In the EMR exposed group, while tissue MDA, NO levels and urinary NAG levels increased (p < 0.0001), the activities of SOD, CAT, and GSH-Px in renal tissue were reduced (p < 0.001). CAPE treatment reversed these effects as well (p < 0.0001, p < 0.001 respectively). In conclusion, the increase in NO and MDA levels of renal tissue, and in urinary NAG with the decrease in renal SOD, CAT, GSH-Px activities demonstrate the role of oxidative mechanisms in 900 MHz mobile phone-induced renal tissue damage, and CAPE, via its free radical scavenging and antioxidant properties, ameliorates oxidative renal damage. These results strongly suggest that CAPE exhibits a protective effect on mobile phone-induced and free radical mediated oxidative renal impairment in rats.     

Caffeic Acid Phenethyl Ester Modulates Gentamicin-Induced Oxidative Nephrotoxicity in Kidney of Rats

In this study, the modulator effect of caffeic acid phenethyl ester (CAPE) on the oxidative nephrotoxicity of gentamicin in the kidneys of rats was investigated by determining indices of lipid peroxidation and the activities of antioxidant enzymes as well as by histological analyses. Forty female Wistar albino rats were randomly divided into four groups, namely control, gentamicin, CAPE, and gentamicin plus CAPE. On the 12th day of the study, all rats were sacrificed and then blood samples and kidneys were taken. Lipid peroxidation and nitric oxide levels, glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) enzyme activities, and histological evaluation were measured in kidneys of rats. Levels of blood urea nitrogen and creatinine were studied in serum. CAPE with gentamicin caused decreases in lipid peroxidation, nitric oxide, urea nitrogen, and creatinine levels, although it caused increases in CAT, GSH-Px, and SOD activities when compared with gentamicin alone. In addition, on histological evaluation, the renal damage caused by gentamicin alone appeared much higher than that caused by CAPE plus gentamicin. It is concluded that oxidative stress plays a critical role in causing gentamicin nephrotoxicity and that this nephrotoxicity may be significantly reduced by CAPE.     

Protective effects of melatonin and caffeic acid phenethyl ester against retinal oxidative stress in long-term use of mobile phone: A comparative study

There are numerous reports on the effects of electromagnetic radiation (EMR) in various cellular systems. Melatonin and caffeic acid phenethyl ester (CAPE), a component of honeybee propolis, were recently found to be potent free radical scavengers and antioxidants. Mechanisms of adverse effects of EMR indicate that reactive oxygen species may play a role in the biological effects of this radiation. The present study was carried out to compare the efficacy of the protective effects of melatonin and CAPE against retinal oxidative stress due to long-term exposure to 900 MHz EMR emitting mobile phones. Melatonin and CAPE were administered daily for 60 days to the rats prior to their EMR exposure during our study. Nitric oxide (NO, an oxidant product) levels and malondialdehyde (MDA, an index of lipid peroxidation), were used as markers of retinal oxidative stress in rats following to use of EMR. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status in retinal tissue. Retinal levels of NO and MDA increased in EMR exposed rats while both melatonin and CAPE caused a significant reduction in the levels of NO and MDA. Likewise, retinal SOD, GSH-Px and CAT activities decreased in EMR exposed animals while melatonin and CAPE caused a significant increase in the activities of these antioxidant enzymes. Treatment of EMR exposed rats with melatonin or CAPE increased the activities of SOD, GSH-Px and CAT to higher levels than those of control rats. In conclusion, melatonin and CAPE reduce retinal oxidative stress after long-term exposure to 900 MHz emitting mobile phone. Nevertheless, there was no statistically significant difference between the efficacies of these two antioxidants against to EMR induced oxidative stress in rat retina. The difference was in only GSH-Px activity in rat retina. Melatonin stimulated the retinal GSH-Px activity more efficiently than CAPE did.     

Caffeic acid phenethyl ester suppresses oxidative stress in Escherichia coli-induced pyelonephritis in rats

Although oxidative damage is known to be involved in inflammatory-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory diseases. Caffeic acid phenethyl ester (CAPE), an active component of propolis from honeybee hives, has antioxidant, anti-inflammatory and antibacterial properties. For that reason, we aimed to investigate the efficiency of CAPE administration in preventing oxidative damage in pyelonephritis (PYN) caused by Escherichia coli. In this study, 35 Wistar rats were grouped as follows: control, PYN 24 h, PYN 48 h, PYN 72 h, CAPE 24 h, CAPE 48 h and CAPE 72 h. E. coli (1 × 10⁹ c.f.u.) were inoculated into the rats in both PYN and CAPE groups via urethral catheterization. Ten μM/kg-body weight CAPE was injected to the rats in all CAPE groups 24 h before E. coli infection, and injections were repeated at 24-h intervals. Rats were sacrificed 24 h, 48 h and 72 h after infection in both PYN and CAPE groups. Malondialdehyde (MDA) and nitric oxide (NO) levels were significantly increased in kidneys of PYN groups. The activities of the antioxidant enzymes, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and xanthine oxidase (XO) were also elevated by E. coli. However, CAPE administration reduced MDA and NO levels, as well as XO activity, although it increased SOD and GSH-Px activities. Histopathological examination showed that CAPE reduced the inflammation grade induced by E. coli. In conclusion, CAPE administrations decrease the oxidative damage occurring in PYN and therefore could be used for medical management of bacterial nephropathy.     

The Activities of Antioxidant Enzymes and the Level of Malondialdehyde in Cerebellum of Rats Subjected to Methotrexate: Protective Effect of Caffeic Acid Phenethyl Ester

Methotrexate (MTX), a folic acid antagonist, is widely used as a cytotoxic chemotherapeutic agent. MTX-associated neurotoxicity is an important clinical problem. The aim of this study was to investigate the role of caffeic acid phenethyl ester (CAPE) on cerebellar oxidative stress induced by MTX in rats. A total of 19 adult male rats were divided into three experimental groups as follows: MTX group (MTX treated), MTX+CAPE group (MTX+CAPE treated), and control group. MTX was administered intraperitoneally (i.p.) with a single dose of 20 mg kg⁻¹ on the second day of experiment. CAPE was administered i.p. with a dose of 10 μmol kg⁻¹ day⁻¹ for 7 days. Malondialdehyde (MDA) levels and activities of superoxide dismutase (SOD) and catalase (CAT) were determined in cerebellar tissue of rats. MTX caused to significant increase in MDA levels (an important marker of lipid peroxidation) in the MTX group compared with the controls (p = 0.006). CAPE significantly reduced the MTX induced lipid peroxidation in the MTX+CAPE group compared to the MTX (p = 0.007). The activities of SOD and CAT were significantly increased in the MTX group when compared with the control group (p = 0.0001, p = 0.004, respectively). The increased activities of these enzymes were significantly reduced by CAPE treatment (p = 0.004, p = 0.034, respectively). As a result, CAPE may protect from oxidative damage caused by MTX treatment in rat cerebellum.     

The Protective Effects of Tea Polyphenols and Schisandrin B on Nephrotoxicity of Mercury

Mercury (Hg) is an occupational and environmental contaminant that is a well-recognized health hazard. To approach the concrete mechanisms of mercury nephrotoxicity and find out a new way to prevent it, the rats were subcutaneously injected with different dosages of mercuric chloride (HgCl₂)—0, 2.2, 4.4, and 8.8 μmol/kg. The levels of Hg, blood urea nitrogen (BUN), urine protein, glutathione (GSH), malondialdehyde (MDA) and activities of N-acetyl-beta-d-glucosaminidase (NAG), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were investigated, and the levels of reactive oxygen species (ROS) and apoptosis and the pathological changes were also observed. In addition, the effects of 1 mmol/kg tea polyphenols (TP) and 0.04 mmol/kg schisandrin B (Sch B) were studied at 8.8 μmol/kg HgCl₂. It was observed that the levels of Hg, BUN, urine protein, GSH, and MDA and activities of NAG, ALP, and LDH increased significantly; the activities of SOD and GSH-Px decreased significantly; the levels of ROS and apoptosis increased obviously; and many pathological changes occurred dose-dependently in the HgCl₂ injection groups. Further investigation indicated that pretreatment with TP and Sch B significantly reversed the toxic effects of HgCl₂. These results suggested that TP and Sch B might antagonize the nephrotoxicity caused by HgCl₂ exposure.     

Protective effect of caffeic acid phenethyl ester (CAPE) on lipid peroxidation and antioxidant enzymes in diabetic rat liver

The aim of this study was to examine the effect of caffeic acid phenethyl ester (CAPE) on lipid peroxidation (LPO) and the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in the liver of streptozotocin (STZ)-induced diabetic rats. Twenty-seven rats were randomly divided into three groups: group I, control non-diabetic rats (n = 9); group II, STZ-induced, untreated diabetic rats (n = 8); group III, STZ-induced, CAPE-treated diabetic rats (n = 10), which were intraperitoneally injected with CAPE (10 microM kg(-1) day(-1)) after 3 days followed by STZ treatment. The liver was excised after 8 weeks of CAPE treatment, the levels of malondialdehyde (MDA) and the activities of SOD, CAT, and GSH-Px in the hepatic tissues of all groups were analyzed. In the untreated diabetic rats, MDA markedly increased in the hepatic tissue compared with the control rats (p < 0.0001). However, MDA levels were reduced to the control level by CAPE. The activities of SOD, CAT, and GSH-Px in the untreated diabetic group were higher than that in the control group (p < 0.0001). The activities of SOD and GSH-Px in the CAPE-treated diabetic group were higher than that in the control group (respectively, p < 0.0001, p < 0.035). There were no significant differences in the activity of CAT between the rats of CAPE-treated diabetic and control groups. Rats in the CAPE-treated diabetic group had reduced activities of SOD and CAT in comparison with the rats of untreated diabetic group (p < 0.0001). There were no significant differences in the activity of GSH-Px between the rats of untreated diabetic and CAPE-treated groups. It is likely that STZ-induced diabetes caused liver damage. In addition, LPO may be one of the molecular mechanisms involved in STZ-induced diabetic damage. CAPE can reduce LPO caused by STZ-induced diabetes.     

Protective effect of caffeic acid phenethyl ester (CAPE) administration on cisplatin-induced oxidative damage to liver in rat

Cisplatin is one of the most active cytotoxic agents in the treatment of cancer. High doses of cisplatin have also been known to produce hepatotoxicity. Several studies suggest that supplementation with an antioxidant can influence cisplatin-induced hepatotoxicity. The present study was designed to determine the effects of cisplatin on the liver oxidant/antioxidant system, and the possible protective effects of caffeic acid phenethyl ester (CAPE) on liver toxicity induced by cisplatin. Twenty-four adult female Wistar albino rats were divided into four groups of six rats each: control, cisplatin, CAPE, and cisplatin+CAPE. Cisplatin and CAPE were injected intraperitoneally. Liver tissue was removed to study the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), myeloperoxidase (MPO), xanthine oxidase (XO), adenosine deaminase (ADA), and the levels of malondialdehyde and nitric oxide (NO). The activities of SOD and GSH-Px increased in the cisplatin+CAPE and CAPE groups compared with the cisplatin group. CAT activity was higher in the cisplatin +CAPE group than the other three groups. XO activity was lower in the cisplatin group than the control group. MPO activity was also increased in the cisplatin group compared to the control and CAPE groups. It can be concluded that CAPE may prevent cisplatin-induced oxidative changes in liver by strengthening the antioxidant defence system by reducing reactive oxygen species and increasing antioxidant enzyme activities.     

Protective effects of caffeic acid phenethyl ester (CAPE) on amikacin-induced nephrotoxicity in rats

Amikacin (AK) has nephrotoxic side effects. AK-induced nephrotoxicity may be the consequence of oxidative stress and so anti-oxidant agents could be useful in reducing AK toxicity. Caffeic acid phenethyl ester (CAPE) was recently shown to have free radical scavenging ability and it reduces lipid peroxidation. For this purpose, the rats were distributed into three groups: (I) injected with vehicle (control); (II) injected (i.p.) with 1.2 g kg(-1) AK at a single dose; (III) injected (i.p.) with AK plus 10 micromol kg(-1) CAPE. Renal morphology was investigated by light microscopy. Tissue samples and trunk blood were also obtained to determine renal malondialdehyde (MDA), blood urea nitrogen (BUN) and creatinine (Cr) levels. MDA production was found to be higher in rats given AK than among control rats. CAPE administration before AK injection caused a significant decrease in MDA production. Morphological tubule damage in rats given AK was severe in the renal cortex, whereas in rats given AK plus CAPE, no histological changes occurred. It is concluded that CAPE could be useful for reducing the nephrotoxic effects of AK. Copyright (c) 2005 John Wiley & Sons, Ltd.     

Caffeic acid phenethyl ester improves oxidative organ damage in rat model of thermal trauma

Severe burn injuries cause functional impairment in distant internal organs. Although this mechanism is not clear, it is possible that free radical toxicity plays an important role. Research in animals and clinical studies have shown that there is a close relationship between a lipid peroxidative reaction and secondary pathological changes following thermal injury. It has been demonstrated that antioxidant treatment prevents oxidative tissue damage associated with thermal trauma. This study was designed to determine the possible protective effect of caffeic acid phenethyl ester (CAPE) treatment against oxidative damage in the kidney and lung induced by thermal injury. Rats were decapitated either 1, 3 or 7 days after burn injury. CAPE was administered intraperitoneally immediately after thermal injury. Kidney and lung tissues were taken for the determination of malondialdehyde (MDA) level, myeloperoxidase (MPO), catalase (CAT), superoxide dismutase (SOD) and xanthine oxidase (XO) activities. Severe skin thermal injury caused a significant decrease in SOD and CAT activities, as well as significant increases in MDA level, XO and MPO activities in tissues during the postburn period. Treatment of rats with CAPE (10 micromol/kg) significantly elevated the decreased SOD and CAT activities, while it decreased MDA levels and MPO as well as XO activity.     

Protective effects of caffeic acid phenethyl ester on iron-induced liver damage in rats

Caffeic acid phenethyl ester (CAPE) is a natural product with potent anti-inflammatory, antitumor, and antioxidant activities, and attenuates inflammation and lipid peroxidation. The purpose of the present study was to investigate the effects of CAPE on iron-induced liver damage. Rats were divided into four groups and treated for 7 days with saline (control group), 10 μmol kg CAPE/day s.c. (CAPE group), 50 mg iron-dextran/kg i.p. (IRON group) and CAPE and iron at the same time (IRON+CAPE group). Seven days later, rats were killed and the livers were excised for biochemical analysis. The administration of IRON alone resulted in higher myeloperoxidase (MPO) activity and lipid peroxidation than in the control and CAPE treatment prevented the increase in MPO activity and malondialdeyde (MDA) level. No differences were observed in all four groups with regards to superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities. Our results collectively suggest that CAPE may be an available agent to protect the liver from injury via inhibition of MPO activity.     

<Emphasis Type="Italic">Undaria pinnatifida</Emphasis> fucoidan extract protects against CCl<Subscript>4</Subscript>-induced oxidative stress

This study was performed to elucidate the effects of Undaria pinnatifida fucoidan extract (UPFE) in preventing CCl₄-induced oxidative stress. UPFE (100 mg/kg) was intraperitoneally administered to rats for 14 days. On day 15, CCl₄ dissolved in olive oil (50% CCl₄) was injected 12 h before they were anesthetized and dissected. To measure UPFE-mediated antioxidation, we examined the levels of glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) in serum, as well as malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in liver homogenates. CCl₄ treatment markedly increased the levels of GOT, GPT, ALP, LDH, and MDA and significantly decreased levels of SOD, CAT, and GPx. UPFE pretreatment decreased levels of GOT, GPT, ALP, LDH, and MDA, by 62.8, 68.5, 41.9, 72.7, and 122%, respectively and increased those of SOD, CAT, and GPx by 111.1, 15.9, and 52.6%, respectively. These results showed that UPFE has antioxidant effects against CCl₄-induced oxidative stress.     

Effect of aerobic exercise intervention on DDT degradation and oxidative stress in rats

Dichlorodiphenyltrichloroethane (DDT) reportedly causes extensively acute or chronic effects to human health. Exercise can generate positive stress. We evaluated the effect of aerobic exercise on DDT degradation and oxidative stress.Main methods: Male Wistar rats were randomly assigned into control (C), DDT without exercise training (D), and DDT plus exercise training (DE) groups. The rats were treated as follows: DDT exposure to D and DE groups at the first 2 weeks; aerobic exercise treatment only to the DE group from the 1st day until the rats are killed. DDT levels in excrements, muscle, liver, serum, and hearts were analyzed. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) levels were determined. Aerobic exercise accelerated the degradation of DDT primarily to DDE due to better oxygen availability and aerobic condition and promoted the degradation of DDT. Cumulative oxidative damage of DDT and exercise led to significant decrease of SOD level. Exercise resulted in consistent increase in SOD activity. Aerobic exercise enhanced activities of CAT and GSH-Px and promoted MDA scavenging. Results suggested that exercise can accelerate adaptive responses to oxidative stress and activate antioxidant enzymes activities. Exercise can also facilitate the reduction of DDT-induced oxidative damage and promoted DDT degradation. This study strongly implicated the positive effect of exercise training on DDT-induced liver oxidative stress.     

全氟辛烷磺酸钾对小鼠肾脏的氧化性损伤

目的:以小鼠肾脏细胞中的活性氧(ROS)、丙二醛(MDA)、谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活力为指标,探讨全氟辛烷磺酸钾(PFOS-K)对小鼠肾脏的氧化性损伤作用。方法:以剂量为6mg/kg·bw、12 mg/kg·bw、24 mg/kg·bw 3个浓度的PFOS-K混悬液,每天分别给小鼠经口灌胃一次,连续染毒20天后检测肾脏脏器系数,以及肾脏中ROS、MDA、GSH含量的变化和SOD、GSH-Px、CAT活性的改变。结果:与阴性对照组相比,在6-24 mg/kg·bw剂量范围内,PFOS-K使小鼠体重下降、肾脏重量增加、肾脏脏器系数增大,且表现出一定的剂量-效应关系(r小鼠体重=-0.905,r肾脏湿重=0.938,r脏器系数=0.936)。PFOS-K使小鼠肾脏内活性氧(ROS)及丙二醛(MDA)含量增多(rROS=0.990,rMDA=0.997)、谷胱甘肽(GSH)含量减少(rGSH=-0.994),超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活力降低(rSOD=-0.917,rGSH-Px=-0.986,rCAT=-0.991)。结论:本试验条件下,PFOS-K致使小鼠肾脏肿大,影响了肾脏的发育;造成了肾脏的氧化性损伤,肾组织内抗氧化酶系统遭到破坏,氧化应激反应增强,具有氧化损伤作用。     

Effect of polyaspartic acid on CdCl2-induced nephrotoxicity in the rat

We produced an animal model of CdCl₂ nephrotoxicity in rats, and treated them with polyaspartic acid (PAA) to prevent renal damage. Male Sprague-Dawley (SD) rats (190–200 g) were used to induce proximal renal tubular damage by daily injection of CdCl₂ 3.0 mg/1,000 g body wt for 2 wk. CdCl₂-exposed SD rats exhibited significant increases in urine volume, urinary excretion ofN-acetyl-β-D-glucosaminidase (NAG), alanine aminopeptidase (AAP), and fractional excretion of sodium (FENa) and a decrease in the percentage of tubular reabsorption of phosphate (%TRP). Of these indicators of proximal tubular function, AAP and %TRP are more sensitive than NAG or FENa. No glycosuria or aminoaciduria, however, were observed. PAA markedly improved these indicators of proximal tubular function. Daily urinary protein excretion and creatinine clearance, on the other hand, did not change after administration of PAA. Cd concentrations in the cortex were 3 times higher than in the medulla, however, there were no differences between Cd-treated rats and PAA-treated rats. Our animal model is an excellent one for determining the effect of cadmium on renal proximal tubule damage. PAA appears to be useful in the treatment of CdCl₂ nephrotoxicity.     

普罗布考对糖尿病大鼠肾组织氧化应激的影响

目的研究普罗布考（Probucol）对糖尿病大鼠肾组织氧化应激的影响。方法采用腹腔注射链脲佐菌素（STZ）建立糖尿病大鼠模型。30只Wistar大鼠分为正常对照组（NC）、糖尿病组（DM）、糖尿病普罗布考治疗组（DP）。8周末称取体重、肾重、计算肾肥大指数（肾重/体重）,检测尿白蛋白排泄率（UAER）;测定各组生化指标包括血糖（BG）、胆固醇（TC）、三酰甘油（TG）、血清肌酐（SCr）、血尿素氮（BUN）;检测肾组织中丙二醛（MDA）的含量及超氧化物歧化酶（SOD）、过氧化氢酶（CAT）与谷胱甘肽过氧化物酶（GSH-Px）活性;肾组织切片行PAS染色分析肾小球面积及肾小球体积。结果 DM组大鼠肾重、肾重/体重、UAER、TC、TG、SCr、BUN、肾小球面积、肾小球体积较NC组均明显增加,DP组上述改变较DM组均明显减轻（P〈0.05）。DP组肾组织中MDA含量明显低于DM组,SOD、CAT、GSH-Px活性明显高于DM组（P〈0.05）。结论普罗布考可能部分通过减轻肾组织氧化应激反应实现对糖尿病大鼠肾脏的保护作用。     

Evaluation of the effects of cadmium on rat liver

Abstact Cadmium is one of the most toxic pollutants in environment. Cadmium accumulation in blood affects the renal cortex and causes renal failure. In this study, we aimed to evaluate the effects of cadmium on rat liver tissue. Eighteen male albino rats aged ten weeks old were used in the study. 15 ppm of cadmium was administered to rats via consumption water daily. At the end of the 30th study day, the animals were killed under ether anesthesia. After the liver tissue samples were taken, histopathological and biochemical examinations were performed. Histopathologic changes have included vacuolar and granular degenerations in hepatocytes, heterochromatic nucleuses and sinusoidal and portal widenings. Central vein diameters were normal in cadmium exposed group. Whereas, there was statistically significant difference between two groups by means of sinusoidal (p< 0.001) and portal triad diameters (p< 0.01). Malondialdehyde (MDA) is an indicator of lipid peroxidation. In this study, MDA was used as a marker of oxidative stress-induced liver impairment in cadmium exposed rats. Superoxide dismutase (SOD) and catalase (CAT) activities were also measured to evaluate the changes in antioxidative system in liver tissues. Current findings showed that MDA levels were increased and SOD and CAT activities were decreased in cadmium exposed group compared to control group. The difference between two groups was statistically significant (pvalues: MDA,p< 0.01; CAT,p< 0.01 and SOD,p< 0.05). In conclusion, these findings suggest the role of oxidative mechanisms in cadmium-induced liver tissue damage     

Protection by ebselen against cisplatin-induced nephrotoxicity: Antioxidant system

This study was designed to investigate the cisplatin-induced alteration in renal antioxidant system and the nephroprotection with ebselen. Male Wistar rats were injected with (1) vehicle control; (2) cisplatin; (3) ebselen; and (4) cisplatin plus ebselen. Rats were sacrificed three days post-treatment and plasma as well as kidney were isolated and analyzed. Plasma creatinine increased 598% following cisplatin administration alone which decreased by 158% with ebselen pretreatment. Cisplatin-treated rats showed a depletion of renal glutathione (GSH) levels (52% of control), while cisplatin plus ebselen injected rats had GSH values close to the controls. Antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities decreased 38, 75 and 62% of control, respectively, and malondialdehyde (MDA) levels increased 174% of control following cisplatin administration, which were restored to control levels after ebselen treatment. The renal platinum level did not significantly change with ebselen pretreatment. This study suggests that the protection offered by ebselen against cisplatin-induced nephrotoxicity is partly related to the sparing of antioxidant system.     

Age-related changes in antioxidant enzyme activities and lipid peroxidation in lungs of control and sulfur dioxide exposed rats

Antioxidant defenses within the lung are pivotal in preventing damage from oxidative toxicants. There have also been several reports with conflicting results on the antioxidant system during aging. In this study, we attempted to investigate age-related alterations in both antioxidant enzyme activities and thiobarbituric acid-reactive substances (TBARS), a product of lipid peroxidation, in the whole lung of control and sulfur dioxide (SO₂) exposed rats of different age groups (3-, 12-, and 24-months-old). Swiss-Albino Male rats were exposed to 10 ppm SO₂ 1 hr/day, 7 days/week for 6 weeks. The antioxidant enzymes examined include Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione S-transferase (GST). A mixed pattern of age-associated alterations in antioxidant activities was observed. SOD, GSH-Px and GST activities were increased with age, but CAT activity was decreased. Lung SOD, GSH-Px and GST activities were also increased in response to SO₂. The level of TBARS was increased with age. SO₂ exposure stimulated lipid peroxide formation in the lung as indicated by an increase in the level of TBARS. These findings suggest that both aging and SO₂ exposure may impose an oxidative stress to the body. We conclude that the increase in the activities of the antioxidant enzymes of the lung during aging, could be interpreted as a positive feedback mechanism in response to rising lipid peroxidation.     

Antioxidative responses and their relation to salt tolerance in <Emphasis Type="Italic">Echinochloa oryzicola</Emphasis> Vasing and <Emphasis Type="Italic">Setaria virdis</Emphasis> (L.) Beauv.

Two gramineous species among wild plants, Echinochloa oryzicola Vasing and Setaria viridis (L.) Beauv., and Oryza sativa L. cv. Nipponbare were subjected to salt stress. The relative growth rate (RGR), Na content, photosynthetic rate, antioxidant enzymes activity (superoxide disumutase (SOD), catalase (CAT), ascorbate peroxidase (APx) and glutathione reductase (GR)), and malondialdehyde (MDA) content in leaves after NaCl treatment were studied. RGR significantly decreased in O. sativa more than in E. oryzicola and S. viridis. Comparatively salt-tolerant S. viridis showed higher growth rate, lower Na accumulation rate in leaves, higher photosynthetic rate, and induced more SOD, CAT, APx, and GR activity and lower increase of MDA content as compared to the salt-sensitive O. sativa. At the same time, the comparatively salt-tolerant E. oryzicola also showed higher growth rate, much lower Na accumulation and no observable increase of MDA content, even though the CAT and APx activities were not induced by salinity. These results suggested that the scavenging system induced by H₂O₂-mediated oxidative damage might, at least in part, play an important role in the mechanism of salt tolerance against cell toxicity of NaCl in some gramineous plants