The effect of vitamin E, probucol, and lovastatin on oxidative status and aortic fatty lesions in hyperlipidemic-diabetic hamsters

Elswefy, Sahar E; Schaefer, Ernst J.; Seman, Leo; Dongen, D. van; Sevanian, Alex; Smith, Donald E.; Ordovas, José M.; Elsweidy, M.; Meydani, Mohsen

doi:10.1016/s0021-9150(99)00331-7

Cited by 44 publications

(39 citation statements)

References 50 publications

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“…A indução de diabetes em hamsteres utilizando STZ pode ser conseguida utilizando doses múltiplas de droga ou em uma dose única (17,22). Em nosso trabalho aplicamos uma dose única de 50 mg/ kg de STZ e observamos um aumento significativo da concentração de glicose sérica desde o terceiro dia após a aplicação.…”

Section: Discussionunclassified

Efeito da estreptozotocina sobre os perfis glicêmico e lipídico e o estresse oxidativo em hamsters

Silva

Lima

Pedrosa

2011

Arq Bras Endocrinol Metab

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RESUMOObjetivo: Este estudo avaliou os efeitos da estreptozotocina nos perfis glicêmico e lipídico e marcadores de estresse oxidativo em hamsteres. Materiais e métodos: Hamsteres machos Golden Syrian foram divididos em dois grupos: grupo diabético (D), que recebeu uma única injeção de estreptozotocina (STZ -50 mg/kg), e grupo controle (C), que recebeu injeção de tampão citrato. Os animais foram eutanasiados após 10 dias de experimento e o sangue, o fígado e rins foram coletados. Resultados: O grupo diabético apresentou níveis maiores de glicose, triacilgliceróis e colesterol séricos e maior concentração de substâncias reativas ao ácido tiobarbitúrico (TBARs) no fígado e nos rins. Também apresentou significativo aumento da concentração de glutationa no fígado e menores atividades da paraoxonase e do superóxido dismutase. Conclusão: Hamsteres fornecem um bom modelo para o diabetes melito do tipo I e estresse oxidativo, similar ao da síndrome humana, e poderão ser adequados para a análise de compostos antidiabéticos. Arq Bras Endocrinol Metab. 2011;55(1):46-53 Descritores Hamsteres; estreptozotocina; estresse oxidativo; antioxidantes ABSTRACT Objective: This study evaluated the effects of streptozotocin on glycemic and lipid profiles and oxidative stress status in hamsters. Materials and methods: Male Golden Syrian hamsters were divided in diabetic group (D) which received a streptozotocin single injection (STZ -50 mg/kg), and control group (C) which received a single injection of the vehicle citrate buffer. Animals were euthanized after 10 days of experiment and blood, liver and kidneys were collected. Results: The diabetic group had higher levels of glucose, triacylglycerols and cholesterol in serum and thiobarbituric acid reactive substances (TBARS) concentration increased in the liver and kidneys. Diabetes induced a significant increase in glutathione concentration in the liver and decreased paraoxonase and superoxide dismutase activities. Conclusion: Hamsters provide a novel animal model for diabetes mellitus and oxidative stress, similar to the human syndrome, which may be suitable for the testing of antidiabetic compounds. Arq Bras Endocrinol Metab. 2011;55 (1) InTRODUçãO O termo diabetes melito (DM) é uma desordem metabólica de múltiplas etiologias caracterizadas por hiperglicemia crônica com distúrbios no metabolismo de carboidratos, lipídios e proteínas, como resultado do defeito na secreção de insulina ou em sua ação ou ambos (1). Há mais de 250 milhões de pessoas em todo o mundo com diabetes e estima-se que a cada 5 segundos surja um novo caso (2). O diabetes pode gerar complicações como retinopatias, nefropatias, neuropatias e distúrbios endócrinos. O papel do estresse oxidativo nessas complicações tem sido alvo de muito interesse (3,4).

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Section: Discussionunclassified

Efeito da estreptozotocina sobre os perfis glicêmico e lipídico e o estresse oxidativo em hamsters

Silva

Lima

Pedrosa

2011

Arq Bras Endocrinol Metab

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“…However, LDL particles are smaller, denser, and more glycated and oxidized in diabetes, making them a risk factor for vascular disease. Together, LDL and VLDL triglycerides impair endothelium-dependent vasodilation by altering NO production (9,10,39,40). Under basal conditions, endothelial NO synthase-3 is targeted to cholesterol-rich membrane domains characterized by the presence of caveolin, which competes with calmodulin for NO synthase binding, perhaps explaining the inverse relationship between circulating cholesterol levels and NO activity (39,41).…”

Section: Discussionmentioning

confidence: 99%

“…Although there may be indications of reduced NO production, enhanced inactivation of NO by reactive oxygen species is probably the most important mechanism by which NO-dependent endothelial function is blunted by diabetes (2). Indeed, antioxidants improve aorta and corpus cavernosum function of diabetic animals (2,4,7,9,16,17).…”

Section: Discussionmentioning

confidence: 99%

Effects of Rosuvastatin on Nitric Oxide–Dependent Function in Aorta and Corpus Cavernosum of Diabetic Mice

2003

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Elevated plasma lipids contribute to neurovascular dysfunction in diabetes. Statins have lipid-lowering properties and can modulate endothelial nitric oxide (NO) bioavailability. The aim was to assess the impact of these factors on autonomic nitrergic nerve and endothelial function. Thus, the effects of diabetes and treatment with the HMG-CoA reductase inhibitor rosuvastatin (RSV) were examined on corpus cavernosum and aorta from streptozotocin-induced diabetic mice in a 4-week prevention study and a 2-week intervention study, following 4 weeks of untreated diabetes. Cotreatment with mevalonate was used to assess the dependence of RSV's effects on HMG-CoA reductase blockade. Diabetes caused a 25% reduction in NO-mediated endotheliumdependent relaxation to acetylcholine for aorta and cavernosum. Relaxations of cavernosum were in the nondiabetic range following prevention or reversal treatment. The aortic deficit was completely prevented and 60% reversed by RSV. Maximum NO-dependent nonadrenergic, noncholinergic nerve-mediated relaxations of cavernosum were reduced 25-33% by diabetes. RSV treatment prevented 75% and reversed 71% of this diabetic deficit. Cotreatment with mevalonate inhibited the beneficial actions of RSV on aorta and cavernosum. Total plasma cholesterol was unaltered by diabetes or treatment. Thus, RSV corrected defective NO-mediated nerve and vascular function in diabetic mice independent of cholesterol lowering but via effects dependent on cholesterol biosynthesis pathway inhibition.

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“…Oxidative stress also is involved in human diseases such as atherosclerosis, cardiovascular and neurodegenerative diseases, and in aging. Vitamin E and carotenoids have clinical uses in diseases associated with reactive oxygen species (5)(6)(7)(8).…”

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confidence: 99%

Interaction between .ALPHA.-Tocopherol, Tocotrienols and Astaxanthin in Liposomes, Subjected to Lipid Peroxidation

et al. 2003

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Vitamin E is a generic term for a-, b-, g-and d-tocopherols and a-, b-, g-and d-tocotrienols, which have saturated and unsaturated phytyl chains, respectively, and differ in the number and position of the methyl groups on the chroman ring. Studies on vitamin E usually are directed to a-tocopherol, which accounts for 90 % of vitamin E in tissues and is believed to have the greatest biological activity. Nowadays the focus on tocopherols is replaced by that on tocotrienols due to increasing evidence indicating that they have stronger activity than tocopherols. For example, a-tocotrienol, unlike a-tocopherol, shows neuroprotective effects on cells (1). a-, g-and d-tocotrienols, and to a lesser extent d-tocopherol, have potent antiproliferative effects on breast cancer cells (2). Astaxanthin, possessing ketoand hydroxygroups in its terminal rings, shows the highest antioxidant activity among carotenoids (3), and protects against reactive oxygen and nitrogen species, No. 7, 347-352 (2003) Abstract: We studied the cooperative interaction between a-tocopherol, tocotrienols and astaxanthin, incorporated in soybean phosphatidylcholine (PC) multilamellar vesicles (MLV) against 2, 2 -azobis (2-amidinopropane) dihydrochloride (AAPH), 2, 2 -azobis (2, 4-dimethylvaleronitrile) (AMVN), or 1, 3-morpholinosydnonimine hydrochloride (SIN-1) induced lipid peroxidation. Tocotrienols spared a-tocopherol consumption in hydrophilic or lipophylic radicals initiated oxidation. The combination of tocotrienols and astaxanthin had the greatest protective effect on a-tocopherol consumption in MLV, oxidized by the hydrophilic radical initiator. a-Tocopherol and tocotrienols protected astaxanthin against AAPH-, AMVN-, and SIN-1-induced oxidations. In the three oxidations a-tocotrienol was consumed first, followed by a-tocopherol and the tocotrienols in the sequence: b > g > d. Astaxanthin was consumed as fast as g-tocotrienol in AAPH oxidation, as fast as a-tocopherol in AMVN oxidation, and before dtocotrienol in SIN-1 oxidation. In conclusion, a-tocopherol, tocotrienols, and astaxanthin cooperated in protecting against MLV lipid peroxidation. a-Tocotrienol was the most effective antioxidant among them. Astaxanthin was as effective as the chain-breaking antioxidants against lipid peroxidation.

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The effect of vitamin E, probucol, and lovastatin on oxidative status and aortic fatty lesions in hyperlipidemic-diabetic hamsters

Cited by 44 publications

References 50 publications

Efeito da estreptozotocina sobre os perfis glicêmico e lipídico e o estresse oxidativo em hamsters

Efeito da estreptozotocina sobre os perfis glicêmico e lipídico e o estresse oxidativo em hamsters

Effects of Rosuvastatin on Nitric Oxide–Dependent Function in Aorta and Corpus Cavernosum of Diabetic Mice

Interaction between .ALPHA.-Tocopherol, Tocotrienols and Astaxanthin in Liposomes, Subjected to Lipid Peroxidation

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