ascorbic-acid and butenolide

ascorbic-acid has been researched along with butenolide* in 3 studies

Other Studies

3 other study(ies) available for ascorbic-acid and butenolide

ArticleYear
Butenolide induced cytotoxicity by disturbing the prooxidant-antioxidant balance, and antioxidants partly quench in human chondrocytes.
    Toxicology in vitro : an international journal published in association with BIBRA, 2009, Volume: 23, Issue:1

    Butenolide (BUT), a mycotoxin produced by Fusarium species, was detected often in corns or grains from endemic Kashin-Beck disease (KBD) areas in China. In this study, we evaluated the cytotoxicity of BUT on chondrocytes and the possible toxic mechanism with the aim of understanding the pathogenesis and of directing future therapeutic interventions for KBD. Exposure of human chondrocytes and engineered cartilage to high concentration of BUT (> 1 microg/ml) resulted in significant cytotoxicity, manifested by losses in cell viability and changes in cell morphology. BUT with high concentration (> 1 microg/ml) also induced significant oxidative damage to chondrocytes in vitro evidenced by increasing both lipid peroxidation and endogenous antioxidants. Furthermore, free radical scavenging agents, such as selenium (Se), vitamin C (VC) and vitamin E (VE), partly blocked BUT-induced oxidative damage. In conclusion, this finding indicates that BUT induces cytotoxicity to human chondrocytes, and the disturbance of prooxidant-antioxidant balance may play a pivotal role in BUT-induced injuries in chondrocytes. Moreover, Se, VC or VE can quench the toxic effects of BUT to a certain extent, which will possibly direct future therapeutic interventions against KBD.

    Topics: 4-Butyrolactone; Ascorbic Acid; Cartilage, Articular; Cell Survival; Cells, Cultured; Chondrocytes; Dose-Response Relationship, Drug; Drug Antagonism; Free Radical Scavengers; Glutathione; Humans; Immunosuppressive Agents; Lipid Peroxidation; Oxidative Stress; Oxidoreductases; Selenium; Tissue Engineering; Vitamin E

2009
In ovo exposure of a Fusarium mycotoxin butenolide induces hepatic and renal oxidative damage in chick embryos, and antioxidants provide protections.
    Toxicology in vitro : an international journal published in association with BIBRA, 2009, Volume: 23, Issue:7

    Butenolide is a mycotoxin produced by several toxigenic Fusarium species. It frequently invades many important grains, and evokes a broad spectrum of toxic effects. For these reasons, butenolide poses a health risk to both humans and animals. However, many toxicology issues of butenolide including targets and mechanisms of toxicity remain to be elucidated so far. The present study therefore attempts to reveal the toxic profile of butenolide from a viewpoint of oxidative damage, using chick embryos as an in vitro model. A single in ovo injection of butenolide resulted in significant oxidative injuries in embryonic livers and kidneys, as manifested by a dose-dependent depletion of sulfhydryl groups, reduction of glutathione peroxidase activity, and increase of thiobarbituric acid reactive substances production, an indicator of lipid peroxidation. In contrast, co-injections of butenolide with antioxidants sodium selenite, vitamin C and a representative antioxidative enzyme superoxide dismutase markedly abated these oxidative toxicities. In conclusion, the present study suggests that oxidative damage may serve as a mediator in the toxicity of butenolide, and amelioration of antioxidant defense capacity by exogenous supplementation may play a role in the prevention and treatment of butenolide intoxication.

    Topics: 4-Butyrolactone; Animals; Antioxidants; Ascorbic Acid; Chick Embryo; Fusarium; Glutathione Peroxidase; Injections; Kidney; Lipid Peroxidation; Liver; Models, Animal; Mycotoxins; Ovum; Oxidative Stress; Protective Agents; Sodium Selenite; Superoxide Dismutase

2009
Lipid peroxidation and antioxidant defense impairment in the hearts of chick embryos induced by in ovo exposure to Fusarium mycotoxin butenolide.
    Toxicon : official journal of the International Society on Toxinology, 2008, Dec-01, Volume: 52, Issue:7

    Fusarium mycotoxin toxicosis has been implicated as an etiological factor for Keshan disease, an endemic cardiomyopathy prevailing in specific regions of China. Butenolide (4-acetamido-4-hydroxy-2-butenoic acid gamma-lactone) is one of the Fusarium mycotoxins frequently detected from the foodstuffs of endemic areas and has been shown to possess the potential to induce cardiotoxicity, implying this mycotoxin might play a role in the occurrence of Keshan disease. The present study was undertaken to further investigate the myocardial toxicity of butenolide from a viewpoint of oxidative damage. A single in ovo injection of butenolide to chick embryos, an excellent in vitro toxicology model resulted in significant oxidative injuries to the myocardium, manifested by a dose-dependent depletion of sulfhydryl groups, reduction of glutathione peroxidase (GPx) activity, and increase of thiobarbituric acid reactive substances production, a hallmark of lipid peroxidation. In contrast, co-injections of butenolide to chick embryos with sodium selenite or vitamin C, two potent antioxidants, markedly abated these oxidative injuries. In conclusion, the present study clearly indicated that butenolide could induce significant myocardial oxidative injuries. The current findings reinforce the hypothesis that toxicosis by Fusarium mycotoxins may be one of the etiological factors for Keshan disease, and oxidative damage is involved in the pathogenesis of myocardial toxicity.

    Topics: 4-Butyrolactone; Animals; Antioxidants; Ascorbic Acid; Chick Embryo; Embryo, Nonmammalian; Fusarium; Glutathione Peroxidase; Heart; Lipid Peroxidation; Mycotoxins; Oxidative Stress; Sodium Selenite; Sulfhydryl Compounds; Toxicity Tests

2008