An extract of Phyllanthus amarus protects mouse chromosomes and intestine from radiation induced damages

We reported earlier on our preliminary study of the radioprotective effect of Phyllanthus amarus (P.amarus) in mice. P.amarus was found to inhibit the myelosuppression and elevated the levels of antioxidant enzymes in the blood and liver. In the present study we have evaluated the protective effect of P.amarus against radiation-induced changes in the intestine and mouse chromosomal damage. P.amarus at concentrations of 250 & 750 mg/Kg. b. wt were found to elevate the antioxidant enzymes in the intestine and decrease the lipid peroxidation levels. Histopathological evaluations of the intestine revealed decreased damage to intestinal cells, demonstrating that P.amarus protected the intestine. The genotoxic effects of radiation on mouse chromosomes were evaluated by assaying the micronuclei formation and chromosomal aberrations. P.amarus was found to protect the clastogenic effects of radiation as seen from decreased number of micronuclei. The administration of P.amarus was also found to decrease the percentage of chromosomal aberrations. Based on our present and previous reports it could be concluded that P.amarus extract has significant radioprotective activity.     

Modulation of haematopoetic system and antioxidant enzymes by Emblica officinalis gaertn and its protective role against gamma-radiation induced damages in mice

The radio protective effect of the fruit pulp of Emblica officinalis Gaertn (Emblica) was studied in adult Swiss albino mice. Mice were treated with 2.5 g/kg b.wt of Emblica for 10 consecutive days before irradiation and exposed to a single dose of 700 rads (7Gy) of radiation after the last dose. One group was given Emblica continuously for another 15 days after irradiation. Changes in the total leukocyte count, bone marrow viability and hemoglobin were studied after whole body irradiation. Administration of Emblica significantly increased these levels, which were lowered by irradiation. Animals were sacrificed at various time points after irradiation and the activities of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX), and glutathione-S-transferase (GST), and levels of glutathione were assayed in the blood. The damage to the cell membrane after whole body irradiation was studied by measuring the tissue lipid peroxides levels. Administration of Emblica significantly enhanced the activity of the various antioxidant enzymes and GST as well as glutathione system in the blood. Treatment with Emblica also lowered the elevated levels of lipid peroxides in the serum. The data clearly indicated that the extract significantly reduced the bioeffects of radiation. Emblica extract may be useful in reducing the side effects produced during therapeutic radiation.     

Influence of Piper betle on hepatic marker enzymes and tissue antioxidant status in ethanol-treated Wistar rats

Piper betle L. is a commonly used masticatory in Asia. This study was carried out to investigate the hepatoprotective and antioxidant properties of P. betle, using ethanol intoxication as a model of hepatotoxic and oxidative damage. Ethanol-treated rats exhibited elevation of hepatic marker enzymes and disturbances in antioxidant defense when compared with normal rats. Oral administration of P. betle extract (100, 200, or 300 mg/kg body weight) for 30 days significantly (P <.05) decreased aspartate aminotransferase (AST), alanine aminotransferase (ALT), thiobarbituric acid reactive substances (TBARS), and lipid hydroperoxides in ethanol treated rats. The extract also improved the tissue antioxidant status by increasing the levels of nonenzymatic antioxidants (reduced glutathione, vitamin C, and vitamin E) and the activities of free radical-detoxifying enzymes such as superoxide dismutase, catalase, and glutathione peroxidase in liver and kidney of ethanol-treated rats. The highest dose of P. betle extract (300 mg/kg body weight) was most effective. The results were comparable with the known hepatoprotective drug, silymarin. These results indicate that P. betle could afford a significant hepatoprotective and antioxidant effect.     

灰树花多糖对糖尿病小鼠的降血糖作用

目的：观察灰树花多糖（GFP）对糖尿病小鼠（DM）的血糖调节作用。方法：将四氧嘧啶按180mg／kgb．wt．剂量腹腔内1次性注射制作糖尿病小鼠模型。实验组分别按750、250、125rng／kgb．wt．三个剂量每天灌服GFP,正常对照组和实验对照组每日灌服相应体积的水,实验周期均为40d。尾静脉采血测小鼠血糖值及糖耐量实验。结果：喂养40d后,250mg／kg．b．wt．剂量组与实验对照组比较,血糖水平和血糖曲线下面积均明显降低（P〈0.05）,750和125mg／kgb．wt．剂量组与实验对照组比较无明显降低（P〉0.05）。结论：灰树花多糖具有降低实验性糖尿病小鼠血糖的作用。     

沙棘提取物对老龄小鼠的抗氧化作用

目的评价沙棘提取物的抗氧化作用。方法采用老龄小鼠模型,设置老龄对照组、溶剂对照组和0.50g/kg BW、1.00g/kg BW、1.50g/kg BW沙棘提取物组,干预30 d后检测各组动物血液丙二醛(MDA)含量和谷胱甘肽过氧化物酶(GSHPX)活性,肝脏谷胱甘肽(GSH)和蛋白质羰基含量。结果与对照组比较,各剂量组10%肝匀浆中蛋白质羰基含量差异无显著性,1.50g/kg BW沙棘提取物组溶血液中MDA含量降低(P<0.05)、GSH-PX活性明显升高(P<0.05)、10%肝匀浆中GSH含量明显升高(P<0.05)。结论在本试验条件下,沙棘提取物能提高老龄小鼠的抗氧化能力。     

Neuroprotective effects of butterbur and rough aster against kainic Acid-induced oxidative stress in mice

The separate and combined neuroprotective effects of rough aster (Aster scaber) and butterbur (Petasite japonicus) extracts against oxidative damage in the brain of mice challenged with kainic acid were examined by comparing behavioral changes and biochemical parameters of oxidative stress. Rough aster butanol extract (400 mg/kg) and/or butterbur butanol extract (150 or 400 mg/kg) were administered to male ICR mice, 6-8 weeks old, through a gavage for 4 days consecutively, and on day 4, kainic acid (50 mg/kg) was administered intraperitoneally. Compared with the vehicle-treated control, no significant changes in body and brain weight were observed in mice administered rough aster or butterbur butanol extract. Administration of kainic acid only, causing a lethality of approximately 54%, resulted in a significant decrease of total glutathione level and increase of thiobarbituric acid-reactive substances (TBARS) value in brain tissue. The administration of butterbur or rough aster extract (400 mg/kg) decreased the lethality (50%) of kainic acid to 25%, alleviated the behavioral signs of neurotoxicity, restored the cytosolic glutathione level of brain homogenate to approximately 80% (P < .05), and reduced kainic acid-induced increases in TBARS values. In contrast to no significant neuroprotection by butterbur extract at a low dose (150 mg/kg), the combination of rough aster extract and butterbur extract reduced the lethality to 12.5%. Moreover, the combination delayed the onset time of behavioral signs by twofold, and significantly preserved the level of cytosolic glutathione peroxidase and glutathione reductase activities. However, the other biochemical parameters were not altered significantly by the combination. Thus, the combination of two vegetable extracts significantly increased the neuroprotective action against kainic acid-induced neurotoxicity. Based on these findings, the combination of butterbur extract and rough aster extract contains a functional agent or agents that protect against oxidative stress in the brain of mice.     

Effect of Piper betle leaf extract on alcoholic toxicity in the rat brain

The protective effect of Piper betle, a commonly used masticatory, has been examined in the brain of ethanol-administered Wistar rats. Brain of ethanol-treated rats exhibited increased levels of lipids, lipid peroxidation, and disturbances in antioxidant defense. Subsequent to the experimental induction of toxicity (i.e., the initial period of 30 days), aqueous P. betle extract was simultaneously administered in three different doses (100, 200, and 300 mg kg(-1)) for 30 days along with the daily dose of alcohol. P. betle coadministration resulted in significant reduction of lipid levels (free fatty acids, cholesterol, and phospholipids) and lipid peroxidation markers such as thiobarbituric acid reactive substances and hydroperoxides. Further, antioxidants, like reduced glutathione, vitamin C, vitamin E, superoxide dismutase, catalase, and glutathione peroxidase, were increased in P. betle-coadministered rats. The higher dose of extract (300 mg kg(-1)) was more effective, and these results indicate the neuroprotective effect of P. betle in ethanol-treated rats.     

Protection against radiation induced hematopoietic damage in bone marrow of Swiss albino mice by Mentha piperita (Linn)

The protective effects of Mentha piperita (Linn) extract against radiation induced hematopoietic damage in bone marrow of Swiss albino mice have been studied. Mice were given either double distilled water or leaf extract of M. piperita orally (1 g/kg b.wt./day) once a day for three consecutive days, and after 30 min of treatments on the third day were exposed to 8 Gy gamma radiation. Mice were autopsied at 12, 24, 48 hrs and 5, 10 and 20 days post-irradiation to evaluate the percentage of bone marrow cells, frequency of micronuclei and erythropoietin level in serum. An exposure to gamma radiation resulted in a significant decline in the number of bone marrow cells such as leucoblasts, myelocytes, metamyelocytes, band/stab forms, polymorphs, pronormoblasts and normoblasts, lymphocytes, and megakaryocytes. Pretreatment with leaf extract of M. piperita followed by radiation exposure resulted in significant increases in the numbers of leucoblasts, myelocytes, metamyelocytes, band/stab forms, polymorphs, pronormoblasts and normoblasts, lymphocytes, and megakaryocytes in bone marrow as compared to the control group. Pretreatment with leaf extract of M. piperita followed by radiation exposure also resulted in significant decreases in micronucleus frequencies in bone marrow of Swiss albino mice. A significant increase in erythropoietin level was observed at all the studied intervals in leaf extract of M. piperita pretreated irradiated animals as compared to control animals (radiation alone). The results of the present investigation suggest the protective effects of leaf extract of M. piperita against radiation induced hematopoietic damage in bone marrow may be attributed to the maintenance of EPO level in Swiss albino mice.     

Protective effects of soybean isoflavone against gamma-irradiation induced damages in mice

In the present work, we investigated the radioprotective efficacy of soybean isoflavone (SI) in mitigating gamma-irradiation-induced oxidative damage to the livers and blood systems of adult Swiss albino mice. We administered various doses of SI (50 mg/kg b.wt, 100 mg/kg b.wt, and 400 mg/kg b.wt) to the mice for seven consecutive days before exposing them to a single dose of 4.56 Gy 60Co-gamma whole-body irradiation. The irradiated mice continued to receive SI for two or seven days before sacrifice. The SI treatments significantly elevated liver catalase (CAT) and glutathione peroxidase (GPx) enzyme activities and mRNA abundances, and decreased the malonaldehyde (MDA) levels. The SI treatments also accelerated the recovery of circulating white blood cells (WBCs) and reticulocytes (RETs) seven days following irradiation. These effects were dose-dependent, and the strongest effect on most biomarkers (but not on histopathology) was seen with an intermediate dose. Our results provide useful information for future investigations, and strongly implicate a clinical application for SI.     

纳米二氧化钛经口暴露对小鼠肝脏的影响

目的 探讨纳米二氧化钛(TiO2 NPs)经口暴露后对小鼠肝脏的影响。方法 60只健康雄性ICR小鼠随机分为对照组、TiO2 NPs (10、50、100) mg/kg·BW染毒组,连续灌胃30 d后,颈椎脱臼处死小鼠,计算小鼠肝脏系数,观察小鼠肝脏组织病理学切片,测定肝组织匀浆中丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST),超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH - PX)、总抗氧化能力(T - AOC)活力以及丙二醛(MDA)含量。结果 与对照组相比,各染毒组小鼠肝脏系数差异无统计学意义(P＞0.05);病理学切片观察各染毒组肝脏组织均可见不同程度肝组织损伤;随着TiO2 NPs染毒剂量的增加,ALT、AST活力以及MDA含量在50、100 mg/kg·BW组升高,SOD活性在100 mg/kg·BW组降低,GSH - PX活性在50、100 mg/kg·BW组降低,T - AOC水平在10、50、100 mg/kg·BW组均降低,差异均具有统计学意义(P＜0.05)。结论 经口暴露TiO2 NPs,可使小鼠肝脏发生氧化应激反应,造成肝脏氧化损伤,并最终导致小鼠肝脏组织结构及功能破坏,具有一定的肝脏毒性作用。     

Protective effect of Raphanus sativus on D-galactosamine induced nephrotoxicity in rats

The aim of the present study was to evaluate nephroprotective effect of Raphanus sativus ethanolic extract (RSEt) on tissue defense system in galactosamine (GalN) induced renal damage in rats. GalN was administered intraperitoneally at a dose of 400 mg/kg/b.w for three alternate days and the renal toxicity was manifested by a significant (P < 0.05) increase in the levels of renal markers such as urea, creatinine and uric acid. This was found to be associated with decreased activities of renal antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx) and glutathione reductase (GR) and depletion of renal reduced glutathione (GSH), vitamin C and vitamin E. Administration of the RSEt (850 mg/kg/body weight, oral) for 15 days to rats reduced the levels of renal markers and significantly increased the level of antioxidants. The activities of gamma glutamyl transpeptidase (GGT) and thiobarbituric acid reactive substances (TBARS) were also decreased in the kidney of RSEt treated group. Renal histology examination confirmed the damage to the kidney as it reveals severe necrosis of the proximal renal tubules with haemorrhage which was ameliorated by the treatment with RSEt. These results suggest that the R. sativus has protective effects on GalN-mediated nephrotoxicity and this may be related to the action of the antioxidant content of the extract.     

Neuroprotective effect of maltol against oxidative stress in brain of mice challenged with kainic acid

The neuroprotective effect of maltol on oxidative damage in the brain of mice challenged with kainic acid was examined. Male ICR mice, 6-8 weeks of age, were administered orally with maltol (50 or 100 mg/kg) for 5 consecutive days. Thirty minutes after the final administration, the animals were challenged s.c. with kainic acid (50 mg/kg), and neurobehavioral activities were monitored. In addition, biomarkers of oxidative stress and neuronal loss in hippocampus for the biochemical and morphological evaluations were analyzed 2 days after the kainic acid challenge. During 5-day treatment with maltol, the body weight gain was not significantly different from that of vehicle-treated control animals. Administration of kainic acid alone induced severe epileptiform seizures, causing a lethality of approximately 50%, and injuries of pyramidals cells in hippocampus of mice survived the challenge. Kainic acid exposure also resulted in marked decreases in total glutathione level and glutathione peroxidase activity, and an increase in thiobarbituric acid-reactive substances (TBARS) value in brain tissues. In comparison, coadministration with maltol (100 mg/kg) remarkably attenuated the neurobehavioral signs and neuronal loss in hippocampus, leading to a decrease in mortality of animals to 12.5% (p < 0.05), although maltol at a dose of 50 mg/kg failed to show any remarkable protection. In addition, the changes in glutathione and TBARS values and glutathione peroxidase activity induced by kainic acid were restored to control levels by pretreatment with maltol (100 mg/kg). On the basis of these results, maltol is suggested to be a functional agent to prevent the oxidative damage in the brain of mice.     

Leaf extract of Moringa oleifera prevents ionizing radiation-induced oxidative stress in mice

The present study evaluated the hepatoprotective effect of aqueous ethanolic Moringa oleifera leaf extract (MoLE) against radiation-induced oxidative stress, which is assessed in terms of inflammation and lipid peroxidation. Swiss albino mice were administered MoLE (300 mg/kg of body weight) for 15 consecutive days before exposing them to a single dose of 5 Gy of ??Co γ-irradiation. Mice were sacrificed at 4 hours after irradiation. Liver was collected for immunoblotting and biochemical tests for the detection of markers of hepatic oxidative stress. Nuclear translocation of nuclear factor kappa B (NF-κB) and lipid peroxidation were augmented, whereas the superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), and ferric reducing antioxidant power (FRAP) values were decreased by radiation exposure. Translocation of NF-κB from cytoplasm to nucleus and lipid peroxidation were found to be inhibited, whereas increases in SOD, CAT, GSH, and FRAP were observed in the mice treated with MoLE prior to irradiation. Therefore pretreatment with MoLE protected against γ-radiation-induced liver damage. The protection may be attributed to the free radical scavenging activity of MoLE, through which it can ameliorate radiation-induced oxidative stress.     

Modulatory effects of Gymnema montanum leaf extract on alloxan-induced oxidative stress in Wistar rats

OBJECTIVES: In light of evidence that some complications of diabetes mellitus may be caused or exacerbated by oxidative damage, we investigated the effect of Gymnema montanum leaf extract (GLEt) on tissue antioxidant defense systems in alloxan-induced diabetes in rats. METHODS: GLEt was administered orally at a doses of 50, 100, and 200 mg/kg of body weight for 30 d, after which liver and kidney tissues were assayed for the degree of lipid peroxidation by means of markers, reduced glutathione content and activities of catalase, superoxide dismutase, glutathione peroxidase, and glutathione-S-transferase. RESULTS: Treatment of diabetic rats with GLEt increased the antioxidant levels. Liver and kidney from diabetic animals exhibited disturbances in antioxidant defense when compared with normal rats. GLEt at a dose of 200 mg/kg of body weight exhibited a significant effect as compared with 50 and 100 mg/kg of body weight. These effects were compared with glibenclamide, a reference drug. CONCLUSIONS: It may be concluded that, in diabetes, liver and kidney tissues are more vulnerable to oxidative stress and show increased lipid peroxidation. The antioxidant responsiveness mediated by G. montanum may be anticipated to have biological significance in eliminating reactive free radicals that may otherwise affect normal cell functioning and provide a scientific rationale for the use of G. montanum as an antidiabetic plant.     

枳实提取物对实验性糖尿病小鼠肝脏抗氧化防御功能的影响

目的研究枳实提取物对试验性糖尿病小鼠肝脏抗氧化能力的影响。方法用高、中、低剂量的枳实提取物治疗糖尿病小鼠5周后,观察其一般状况、肝脏的抗氧化能力及肝脏组织形态学变化。结果枳实提取物治疗组,与糖尿病模型组比较,血糖水平显著降低(P<0.05),谷胱甘肽含量(GSH)显著增加(P<0.05),谷胱甘肽过氧化物酶活性、丙二醛和NO含量显著降低(P<0.01),超过氧化物歧化酶活性有所增加。光镜下枳实提取物治疗组肝组织细胞损伤较糖尿病组降低。结论枳实提取物具有增强肝脏的抗氧化能力,降低肝细胞损伤作用。     

Hypoglycemic and antioxidant effects of Daraesoon (Actinidia arguta shoot) in animal models of diabetes mellitus

BACKGROUND/OBJECTIVES

The primary objective of the treatment of diabetes mellitus is the attainment of glycemic control. Hyperglycemia increases oxidative stress which contributes to the progression of diabetic complications. Thus, the purpose of this study was to investigate the hypoglycemic and antioxidant effects of Daraesoon (Actinidia arguta shoot) in animal models of diabetes mellitus.

MATERIALS/METHODS

Rats with streptozotocin-induced diabetes received an oral administration of a starch solution (1 g/kg) either with or without a 70% ethanol extract of Daraesoon (400 mg/kg) or acarbose (40 mg/kg) after an overnight fast and their postprandial blood glucose levels were measured. Five-week-old C57BL/6J mice were fed either a basal or high-fat/high-sucrose (HFHS) diet with or without Daraesoon extract (0.4%) or acarbose (0.04%) for 12 weeks after 1 week of adaptation to determine the effects of the chronic consumption of Daraesoon on fasting hyperglycemia and antioxidant status.

RESULTS

Compared to the control group, rats that received Daraesoon extract (400 mg/kg) or acarbose (40 mg/kg) exhibited a significant reduction in the area under the postprandial glucose response curve after the oral ingestion of starch. Additionally, the long-term consumption of Daraesoon extract or acarbose significantly decreased serum glucose and insulin levels as well as small intestinal maltase activity in HFHS-fed mice. Furthermore, the consumption of Daraesoon extract significantly reduced thiobarbituric acid reactive substances and increased glutathione levels in the livers of HFHS-fed mice compared to HFHS-fed mice that did not ingest Daraesoon.

CONCLUSIONS

Daraesoon effectively suppressed postprandial hyperglycemia via the inhibition of α-glucosidase in STZ-induced diabetic rats. Chronic consumption of Daraesoon alleviated fasting hyperglycemia and oxidative stress in mice fed a HFHS diet.     

Neuroprotective Effect of Maltol Against Oxidative Stress in Brain of Mice Challenged with Kainic Acid

Abstract

The neuroprotective effect of maltol on oxidative damage in the brain of mice challenged with kainic acid was examined. Male ICR mice, 6-8 weeks of age, were administered orally with maltol (50 or 100 mg/kg) for 5 consecutive days. Thirty minutes after the final administration, the animals were challenged s.c. with kainic acid (50 mg/kg), and neurobehavioral activities were monitored. In addition, biomarkers of oxidative stress and neuronal loss in hippocampus for the biochemical and morphological evaluations were analyzed 2 days after the kainic acid challenge. During 5-day treatment with maltol, the body weight gain was not significantly different from that of vehicle-treated control animals. Administration of kainic acid alone induced severe epileptiform seizures, causing a lethality of approximately 50%, and injuries of pyramidals cells in hippocampus of mice survived the challenge. Kainic acid exposure also resulted in marked decreases in total glutathione level and glutathione peroxidase activity, and an increase in thiobarbituric acid-reactive substances (TBARS) value in brain tissues. In comparison, coadministration with maltol (100 mg/kg) remarkably attenuated the neurobehavioral signs and neuronal loss in hippocampus, leading to a decrease in mortality of animals to 12.5% (p<0.05), although maltol at a dose of 50 mg/kg failed to show any remarkable protection. In addition, the changes in glutathione and TBARS values and glutathione peroxidase activity induced by kainic acid were restored to control levels by pretreatment with maltol (100 mg/kg). On the basis of these results, maltol is suggested to be a functional agent to prevent the oxidative damage in the brain of mice.     

Changes in liver enzyme activity in the teleost Sparus aurata in response to cadmium intoxication.

Enzyme activity modulation by cadmium in the liver of the teleost fish Sparus aurata was investigated in vivo following 3 and 6 days of CdCl2 administration (2.5 mg/kg body wt). The specific activities of the mitochondrial enzymes NAD-isocitrate dehydrogenase, succinate dehydrogenase, and malate dehydrogenase were stimulated by approximately 20% after 3 days administration and were further increased (by about 40%) after 6 days treatment. In comparison with these enzymes, the activities of glutamate-oxaloacetate transaminase (GOT) and glutamate-pyruvate transaminase (GPT) in mitochondria were less stimulated after the two indicated intervals of treatment. Cadmium significantly reduced the activities of liver cytoplasmic GOT and GPT while a simultaneous increase occurred in the serum activities of these same enzymes. The activity of liver NADPH-cytochrome P450 reductase was stimulated by 25 and 40% after 3 and 6 days cadmium intoxication, respectively. Lastly, the antioxidant enzymes glutathione peroxidase and glutathione reductase in liver and catalase in both liver and blood were strongly reduced after 3 and 6 days cadmium administration. These data suggest that cadmium in fish hepatocytes alters cell membrane structure and concomitantly induces some perturbation in the integrity of the mitochondrial membrane.     

Pomegranate seed extract attenuates chemotherapy-induced acute nephrotoxicity and hepatotoxicity in rats

Cisplatin (CDDP), one of the most active cytotoxic agents against cancer, has adverse side effects, such as nephrotoxicity and hepatotoxicity. The present study was designed to investigate the potential protective effect of pomegranate seed extract (PSE) against oxidative stress caused by CDDP injury of the kidneys and liver by measuring tissue biochemical and antioxidant variables and immunohistochemically testing caspase-3-positive cells. Twenty-four Sprague-Dawley rats were divided into 4 groups: control; CDDP: injected intraperitoneally with CDDP (7 mg/kg body weight, single dose); PSE: treated for 15 consecutive days by gavage with PSE (300 mg/kg per day); and PSE+CDDP: treated by gavage with PSE 15 days after a single injection of CDDP. The degree of protection against CDDP injury afforded by PSE was evaluated by determining the levels of malondialdehyde as a measure of lipid peroxidation. The levels of glutathione and activities of glutathione peroxidase, glutathione S-transferase, and superoxide dismutase were estimated from liver and kidney homogenates; the liver and kidney were also histologically examined. PSE elicited a significant protective effect toward liver and kidney by decreasing the level of lipid peroxidation; elevating the levels of glutathione S-transferase; and increasing the activities of glutathione peroxidase, glutathione S-transferase, and superoxide dismutase. These biochemical observations were supported by immunohistochemical findings and suggested that PSE significantly attenuated nephrotoxicity and hepatotoxicity by the way of its antioxidant, radical-scavenging, and antiapoptotic effects. This PSE extract could be used as a dietary supplement in patients receiving chemotherapy medications.     

Ascorbic acid does not increase the oxidative stress induced by dietary iron in C3H mice

Iron is a potent prooxidant that can induce lipid peroxidation. Ascorbic acid, a potent antioxidant, has prooxidant effects in the presence of iron in vitro. We investigated whether ascorbic acid and iron co-supplementation in ascorbic acid-sufficient mice increases hepatic oxidative stress. C3H/He mice were fed diets supplemented with iron to 100 mg/kg diet or 300 mg/kg diet with or without ascorbic acid (15 g/kg diet) for 3 wk. Liver iron concentration, malondialdehyde (MDA), glutathione (GSH), glutathione S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) were measured. High dietary iron increased liver iron concentrations slightly (P < 0.05), whereas it dramatically increased hepatic MDA (P < 0.0001). Ascorbic acid increased MDA but only in mice fed the low-iron diet (P < 0.05). The high-iron diet reduced GPx (P < 0.0001), CAT (P < 0.0005), SOD (P < 0.05), and GST (P < 0.005) activities regardless of ascorbic acid supplementation. In contrast, ascorbic acid reduced GPx (P < 0.0001) and CAT (P < 0.05) activities only in mice fed the low-iron diet. In conclusion, ascorbic acid supplementation can have prooxidant effects in the liver. However, ascorbic acid does not further increase the oxidative stress induced by increased dietary iron.