Dermal toxicity of Fusarium toxins in combinations

Bhavanishankar, T. N.; Ramesh, H. P.; Shantha, T.

doi:10.1007/bf00316641

Cited by 36 publications

(12 citation statements)

References 12 publications

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“…Erythema and induration were observed on skin patches treated with the toxins. These findings correlated histologically with the thickening of stratum malpighii, mild to moderate degeneration of fibrocytes, and cellular infiltration (22).…”

Section: Pathogenesis Of Infectionmentioning

confidence: 60%

Taxonomy, biology, and clinical aspects of Fusarium species

1994

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There are several taxonomic systems available for identifying Fusarium species. The philosophy used in each taxonomic system is discussed as well as problems encountered in working with Fusarium species in culture. Fusarium species are toxigenic, and the mycotoxins produced by these organisms are often associated with animal and human diseases. The implications for the association of the carcinogens, fumonisins, produced by Fusarium moniliforme and other Fusarium species with human diseases are discussed. Foreign-body-associated fusarial infection such as keratitis in contact lens wearers, onychomycosis, skin infections, and disseminated multiorgan infections are discussed. Disseminated fusarial hyalohyphomycosis has emerged as a significant, usually fatal infection in the immunocompromised host. Successful outcome is determined by the degree of immunosuppression, the extent of the infection, and the presence of a removable focus such as an indwelling central venous catheter. These infections may be clinically suspected on the basis of a constellation of clinical and laboratory findings, which should lead to prompt therapy, probably with one of the newer antifungal agents. Perhaps the use of such agents or the use of colony-stimulating factors may improve the outcome of this devastating infection. However, until new approaches for treatment develop, effective preventive measures are urgently needed.

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Section: Pathogenesis Of Infectionmentioning

confidence: 60%

Taxonomy, biology, and clinical aspects of Fusarium species

1994

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“…Ingestion of DON, commonly referred to as vomitoxin, or 15 acetyl-DON could produce the symptoms described above as characteristic of trichothecene mycotoxins. (26,(28)(29)(30) The health effects from respiratory exposures to mycotoxins is an area that is less widely studied than the health effects from mycotoxin ingestion. Since mycotoxins are largely nonvolatile, most respiratory exposure to mycotoxins would occur by inhalation of aerosolized spores, hyphae, and small particles of fungal substrate.…”

Section: Mycotoxinsmentioning

confidence: 99%

HETA 94-0033-2552, Ladish Malting Co., Jefferson, Wisconsin.

1996

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“…(Cole and Cox 1981;Thrane 2001). There is increasing evidence that butenolide can induce diverse toxicities, such as cytotoxicity in several cell lines (Vesonder et al 1993), dermal toxicity in guinea pigs characterized by erythema and induration on skin (Bhavanishankar et al 1988), and subacute inhalation toxicity in hamsters, as shown by eye irritation, salivation, increased liver weight, and growth retardation (Feron et al 1979). Keshan disease is a well-known endemic cardiomyopathy which is prevalent in certain areas of China.…”

Section: Introductionmentioning

confidence: 99%

Effects ofFusariumMycotoxin Butenolide on Myocardial Mitochondria In Vitro

Wang

Liu

Peng

2009

Toxicology Mechanisms and Methods

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Fusarium mycotoxin toxicosis has been implicated in the etiology of Keshan disease, an endemic mitochondrial cardiomyopathy prevailing in certain areas of China. Butenolide (4-acetamido-4-hydroxy-2-butenoic acid gamma-lactone) is one of the Fusarium mycotoxins which are frequently detected from cereal grains in endemic areas. A recent study indicates that this mycotoxin induces rat cardiotoxicity, but its effect on the myocardial mitochondria remains unclear. The present study is therefore undertaken to explore the toxic effect potential of butenolide on the myocardial mitochondria. Exposure of cultured cardiac myocytes to 50 microg/ml of butenolide provoked dissipation of mitochondrial membrane potential. Incubation of isolated rat myocardial mitochondria with butenolide of 100 microg/ml for 60 min resulted in mitochondrial swelling, indicating the occurrence of mitochondrial permeability transition. Furthermore, marked oxidative damage in myocardial mitochondria was observed after incubation of isolated myocardial mitochondria with butenolide ranging from 0 to 50 microg/ml for 60 min, as manifested by concentration-dependent increases in the production of thiobarbituric acid reactive substances, the indicator of lipid peroxidation. Contrarily, a representative antioxidant glutathione significantly alleviated this oxidative mitochondrial damage induced by butenolide. In conclusion, these observations clearly show that butenolide can induce dysfunction of myocardial mitochondria, and oxidative damage appears to play a crucial role in these deleterious effects. The present study supports the hypothesis that mycotoxin toxicosis is a probable etiological factor of Keshan disease, the mitochondrial cardiomyopathy.

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Dermal toxicity of Fusarium toxins in combinations

Cited by 36 publications

References 12 publications

Taxonomy, biology, and clinical aspects of Fusarium species

Taxonomy, biology, and clinical aspects of Fusarium species

HETA 94-0033-2552, Ladish Malting Co., Jefferson, Wisconsin.

Effects ofFusariumMycotoxin Butenolide on Myocardial Mitochondria In Vitro

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