Sung, Ji Hoon;Jo, Young Soo;Kim, Su Jin;Ryu, Jeong Soo;Kim, Myung Chul;Ko, Hyun Ju;Sim, Sang Soo
The Korean Journal of Physiology and Pharmacology
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v.17
no.4
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pp.339-345
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2013
We investigated the antihypertensive effect of lutein on $N^G$-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertensive rats. Daily oral administration of L-NAME (40 mg/kg)-induced a rapid progressive increase in mean arterial pressure (MAP). L-NAME significantly increased MAP from the first week compared to that in the control and reached $193.3{\pm}9.6$ mmHg at the end of treatment. MAP in the lutein groups was dose-dependently lower than that in the L-NAME group. Similar results were observed for systolic and diastolic blood pressure of L-NAME-induced hypertensive rats. The control group showed little change in heart rate for 3 weeks, whereas L-NAME significantly reduced heart rate from $434{\pm}26$ to $376{\pm}33$ beats/min. Lutein (2 mg/kg) significantly prevented the reduced heart rate induced by L-NAME. L-NAME caused hypertrophy of heart and kidney, and increased plasma lipid peroxidation four-fold but significantly reduced plasma nitrite and glutathione concentrations, which were significantly prevented by lutein in a dose-dependent manner. These findings suggest that lutein affords significant antihypertensive and antioxidant effects against L-NAME-induced hypertension in rats.
The present study was investigated to elucidate the effects of chlorambucil the heart tissue of various-aged rats. The male rats ranging from 3 to 36 months were used. The cytochemical and biochemical changes in myocardium of the rats were studied in the aspect of free radical roles in aging process. With the goals of evaluating the potential roles of free radicals in aging process, evidence was shought for alterations of myocardial lipid peroxide levels in control and chlorambucil treated rats. The result are summarized as follows: 1. Cytochemical studies showed that the activities of $Mg^{++}$-ATPase and succinic dehydrogenase increased with age. However, these enzyme activities were decreased with treatment of chlorambucil, when compared with control group. Interestingly it was observed that chlorambucil treatment increased the activity of acid phosphatase from 6 months upto 18 months, and decreased after 18 months. 2. The lipid peroxide level in myocatdium was increased with age; chlorambucil-treated group was higher than that of control group. 3. Age-dependent increase in activities of monoamine oxidase, xanthine oxidase and catalase was observed. But the increase of catalase activity was higher than that of monoamine oxidase and xanthine oxidase activity in control group. However, in chlorambucil-treated group, age-dependent decrease of these enzyme activities was observed, and catalase activity was more significant particularly with regard to other enzymes. In consequently, the morphological alterationsof myocardium due to chlorambucil treatment was exclusively observed. We demonstrate that this alteration is occured by lipid peroxidation upon chlorambucil treatment.
The antioxidative effects of fermented milk, mushroom extract and fermented milk containing its extract (Lentinus edodes, Ganoderna lucidum, and Pleurotus ostreatus) on the lipid peroxidation in the tissues of female Sprague-Dawley rats and on the DPPH ($\alpha,\alpha$' -diphenyl-$\beta$-picrylhydrazyl) radical donating ability were studied. The total concentrations of polyphenolic compound in Lentinus edodes, Ganoderma lucidum and Pleurotus ostreatus were 0.34, 0.20 and 0.34%, respectively. The DPPH donating abilities of mushroom extract, fermented milk, fermented milk containing its extract and BHT (butylated hydorxytoluene) as standard were 33.9, 34.9, 51.9 and 95.6%, respectively. Experimental diet groups were divided into five groups: the normal diet (ND), the cholesterol diet (CD), and cholesterol + fermented milk diet (CDFM), cholesterol + mushroom extract diet (CDME) and cholesterol + fermented milk containing mushroom extract diet (CDFMME). The concentrations of lipid peroxide in liver and its microsome were significantly lower in both CDFM and CDFMME groups than in the other groups. The kidney concentration of lipid peroxide was significantly higher in the CD group than in the ND group, but this rise were significantly decreased in the CDFM and CDFMME groups. Meanwhile, the concentrations of heart and spleen and their fractions were not significantly different among dietary groups. This study was suggested that the fermented milk diet containing mushroom extract effectively reduced the lipid peroxidation in liver and kidney of cholesterol-fed female rats.
Adriamycin is a commonly used chemotherapeutic agent for cancer, including acute leukemia, lymphoma, and a number of solid human tumors. However, recent studies have recognized severe cardiotoxicity after an acute dose, which are likely the result of generation of free radicals and lipid peroxidation. Therefore, the clinical uses of adriamycin have been limited. Melatonin, the pineal gland hormone known for its ability to modulate circardian rhythm, has recently been studied in its several functions, including cancer growth inhibition, stimulating the immune system, and acting as an antioxidant and radical scavenging effects. In the present study, we evaluated the effect of melatonin administration on adriamycin-induced cardiotoxicity in rat. Heart slices were prepared using a Stadie-Riggs microtome for the measurement of malondialdehyde (MDA) content used as an index of lipid peroxidation and lactate dehydrogenase (LDH) release as an indicator of lethal cell injury. Serious adriamycin-induced lethality was observed in rat by a single intraperitoneal injection in a dose-dependent manner. A single injection of adriamycin (25 mg/kg, i.p.) induced a lethality rate of 86%, with melatonin (10 mg/kg s.c. for 6 days) treatment reducing the adriamycin-induced lethality rate to 20%. The severe body weight loss caused by adriamycin was also significantly attenuated by melatonin treatment. Treatment of melatonin marked reduced adriamycin-induced the levels of MDA formation and LDH release. A cell damage indicated by the loss of myofibrils, swelling of the mitochondria as well as cytoplasmic vacuolization was seen in adriamycin-treated group. Melatonin attenuated the adriamycin-induced structural alterations. These data provide evidence that melatonin prevents adriamycin-induced cardiotoxicity and might serve as a combination with adriamycin to limit free radical-mediated cardiotoxicity.
The effect of antioxidants on the myocardial cellular damage which occurs during reoxygenation of hypoxic myocardium was examined in isolated rat hearts. The roles of oxygen free radical and lipid peroxidation in reoxygenation injury of myocardium were also investigated. In Langenorff preparation of isolated rat heart, which was made hypoxic by perfusion with the substrate free, hypoxic cardioplegic solution ($37^{\circ}C$, 90 min), the release of cytosolic enzymes (creatine phosphokinase, lactic dehydrogenase) and a lipid peroxidation product, malondialdehyde into the coronary effluent were abruptly increased by reoxygenation. The release of enzymes was closely parallel to that of MDA. These increases of enzymes and lipid peroxidation product were suppressed to various degrees in the presence of scavengers of superoxide anion (superoxide dismutase, 10,000 U), hydrogen peroxide (catalase, 25,000 U) and hydroxyl radical (dimethyl sulfoxide, 10%). A natural antioxidant, ${\alpha}-tocopherol$(4.5 uM) and a synthetic one, butylated hydroxytoluene (2 uM) suppressed the release of cytosolic enzymes with the concomittent reduction of lipid peroxidation as measured by malondialdehyde release into the coronary effluent. These effects of antioxidants were dose dependent, and were more pronounced when the antioxidants were administered throughout hypoxic and reoxygenation periods than given during reoxygenation period only. These results suggest that cytotoxic oxygen free radicals produced in the myocardium during reoxygenation may be responsible fur the myocardial cellular injury by enhancing the lipid peroxidation of cellular membranes. Furthermore, the antioxidants may exert protective effect against reoxygenation damage of hypoxic myocardium through the inhibition of lipid peroxidation reaction.
The antioxidative activities of capsaicin (Cap, 0.02 and 0.04%) on the lipid peroxidation of tissues in male Sprague Dawley rats fed diets with or without orotic acid (1.0%, w/w) were studied in vivo system by measuring thiobarbituric acid reactive substances (TBARS) concentrations. Body weight gain, food intakes, food efficiency ratio and the relative tissues weights of brain, kidney, spleen, heart, and testis were not significantly different among dietary groups. Relative weights of liver were higher in the OA group than that in the other groups. TBARS concentrations in liver were significantly higher in the OA or 0.04% Cap groups than in the normal group, while this raise was not observed 0.02% Cap group. A significant increase in TBARS concentrations was found in the liver of the OA +0.04% Cap group compared with the OA or the 0.04% Cap groups. Nonheme iron concentrations were significantly higher in the liver of the OA, 0.04% Cap, OA+0.02% Cap, OA+0.04% Cap groups than that in the normal group. TBARS concentrations in kidney were lower in the 0.02% or 0.04% Cap groups than that in the normal group, but this concentrations were higher in either the OA, OA+0.02% Cap or OA+0.04% Cap groups than that in the normal group. Meanwhile, TBARS concentrations of brain, spleen, heart and testis were not significantly different among groups. The present study suggested that the lipid peroxidation was increased in the rats liver fed diet with erotic acid, and the simultaneous supplementation of capsaicin further enhanced.
Glutathione is a well-known chemotherapeutic agent and a popular nutritional supplement for liver disease and oxidative stress. Our previous studies reported the suppressive effects of the glutathione-enriched Saccharomyces cerevisiae FF-8 (FF-8) strain on carbon tetrachloride- and alcohol-induced oxidative stress in rats. The purpose of the current study was to investigate the effect of the FF-8 strain on lipid peroxidation in tissues of rats with orotic acid (OA)-induced fatty liver. OA treatment showed a significant decrease in body weight gain compared to the normal diet, and simultaneous addition of FF-8 and OA had the same effect. OA treatment produced an increase in liver weight, however, this also increased with simultaneous addition of FF-8 and OA. Liver lipid peroxidation was significantly increased by OA, but was significantly decreased by FF-8 strain treatment. This same tendency was found in the kidney and heart. Concentration levels of hepatic glutathione and zinc are known to be closely associated with the antioxidant system, and OA treatment led to reductions in liver glutathione and zinc concentrations, whereas these were significantly increased by FF-8 strain treatment in OA feeding rats. These results suggest that the glutathione-enriched S. cerevisiae FF-8 strain may positively mediate orotic acid-induced oxidative stress by enhancing glutathione and zinc levels in rat livers.
Lipopretein(a)[Lp(a)] is a macromolecular complex found in human plasma that combines structural elements composed of LDL and apo(a), and that is associated with premature coronary heart disease and stroke. In this study, various samples which consisted of normal and abnormal LDL and LP(a) were selected for compar-ison. The above samples were incubated with copper in order to oxidize and to compare atheroma formation, in vitro and free radical formation of Lp(a) was decreased compared to purified LDl. And LDL or Lp(a) from a 40 year old donor was higher in the free radical formation than that fro, a 20 years old donor. In order to investigate the macrophage foam cell formation, oxidized LDL of Lp(a) was incubated with human monocyte derived macrophage(HMDM). Oxidized samples enhanced on acceptability f foam cell formation by HMDM were compared to the control group. Also, structural change of LDL and Lp(a) against oxidation times were found from HPLC mapping.
Doxorubicin induces oxidative stress leading to cardiotoxicity causing electrocardiogram abnormalities and increases in biomarkers associated with toxicity. Green tea extract (GTE) is reported to possess antioxidant activity mainly via its polyphenolic constituent, catechins. This study was intended to determine the effect of various doses of GTE (25, 50 and 100 mg/kg/day p.o. for 30 days) on doxorubicin-induced electrocardiographic and biochemical changes in rat heart. The latter included lactate dehydrogenase, creatine kinase, and glutamic oxaloacetate transaminase in serum and superoxide dismutase, catalase, and reduced glutathione, as well as membrane bound enzymes like $Na^+K^+ATPase,\;Ca^{2+}ATPase,\;Mg^{2+}ATPase$ and decreased lipid peroxidation in heart tissue Results demonstrated that rats which received GTE were less susceptible to such changes indicating protection afforded by GTE.
Journal of the Korean Society of Food Science and Nutrition
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v.20
no.4
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pp.320-328
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1991
The present study was designed to evaluate the effects of dietary vitamin E and coenzyme $Q_{10}$ supplementation on adriamycin (ADR) -induced lipid petoxidation in rats. After feeding the experimental diets for e weeks. Ann treatment significantly decreased growth performance of rats. But this decrement was not modified by supplementation of vitamin E or coenzyme $Q_{10}$ . Lipid peroxide values of plasma and heart mitochondria were elevated by Ann treatment. But these values were significantly decreased according to vitamin E or coenzyme $Q_{10}$ supplementation. Adriamycin treatment elevated glutathione peroxidase (GSH-Px) activity of rats, but this increment was modified by vitamin E supplementation. There was a tendency of higher superoxide dismutase (SOD) activity in ADR-treated rats. However, vitamin E or coenzyme $Q_{10}$ administration reduced this enzyme activity. With ADR treatment, arachidonic acid (20 : 4) was greatly increased, but docosahexaenoic acid (22 : 6) was not detected. Arachidonic acid was decreased and docosahexaenoic acid increased by supplementation of higher level of vitamin E or coenzyme $Q_{10}$ . Present data showed that dietary vitamin E and coenzyme $Q_{10}$ influenced on ADR-induced lipid peroxidation in rats, and also the degree of antioxidative effect was greater in vitamin E-supplemented rats.
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