Inhibition of the glycogen phosphorylase system during ochratoxicosis in chickens

Warren, M F; Hamilton, Pat B.

doi:10.1128/aem.40.3.523-525.1980

Cited by 8 publications

(1 citation statement)

References 20 publications

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“…cyclic AMP-dependent protein kinase deficiency, as the diagnosis of this disorder. This is supported by their enzymatic studies which show that ochratoxin A interferes with protein kinase activity (Warren and Hamilton, 1980). These results are based on the assumption that the kinetics and in particular the pH optima of phosphorylated and non-phosphorylated phosphorylase kinase are the same in chicken and man, which remains to be demonstrated.…”

Section: Induced Gsd-like Conditionsmentioning

confidence: 87%

Glycogen storage diseases in animals and their potential value as models of human disease

Walvoort

1982

J of Inher Metab Disea

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Glycogen storage diseases (GSD) are inborn errors of glycogen metabolism. Of the eight human GSD types in which the enzymatic deficiency has been identified, spontaneous animal counterparts have been reported for GSD I (glucose-6-phosphatase deficiency) in the mouse, for GSD II (acid alpha-glucosidase deficiency) in the dog, in cattle and in the quail, for GSD III (debrancher enzyme deficiency) in the dog and for GSD VIII (phosphorylase kinase deficiency) in the rat and the mouse. Experimentally induced GSD-like conditions have been described in the rat (Acarbose-induced GSD II-like conditions, iodoacetate-induced symptoms of myophosphorylase (GSD V) and myophosphofructokinase (GSD VII) deficiency) and the chicken (ochratoxin A-induced symptoms of cyclic AMP-dependent protein kinase deficiency). Enzymatic defects that are typical of the human GSD types have not been clearly identified in the induced animal conditions. The homology of animal and human GSD types is discussed. It is concluded that clinical, pathogenic and therapeutic studies of GSD may benefit from the use of animal models. For genetic studies of human GSD these models may prove to be of limited value, as the picture of several human GSD types is already obscured by genetic heterogeneity.

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Section: Induced Gsd-like Conditionsmentioning

confidence: 87%

Glycogen storage diseases in animals and their potential value as models of human disease

Walvoort

1982

J of Inher Metab Disea

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Maternal protein deprivation enhances the teratogenicity of ochratoxin a in mice

Singh

Hood

1985

Teratology

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Teratogenic effects of the mycotoxin ochratoxin A (OA) were investigated in protein-deprived mice. Pregnant CD-1 mice were assigned to control (26%), 16%, 8%, and 4% protein diet groups and treated by gavage with 0, 2, or 3 mg/kg OA on gestation day 8 (plug = day 1). They were killed on day 18 and subjected to teratological examination. OA treatment decreased prenatal survival, particularly at the two lowest dietary protein levels. OA at the higher dose also inhibited fetal growth in all groups, with a similar effect at the low dose in the 16% and 4% protein groups. Gross malformations associated with OA were inversely related to dietary protein levels; for example, 26% and 100% of the litters were affected in the 26% and 4% protein groups, respectively, at the high OA dose. A similar trend was also seen for skeletal malformations and variations. Thus maternal protein deprivation was seen to exacerbate adverse effects of OA in a developing mammal. Such results may have implications for areas where lack of adequate food supply may cause consumption of moldy grain by women or domestic animals already living on a protein-deficient diet.

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Histochemical/histoenzymic studies in broiler chicks fed aflatoxin, ochratoxin and inoculated with inclusion body hepatitis virus singly and in concurrence

Singh

Roy

et al. 1994

Mycopathologia

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The effect of feeding mycotoxins, i.e. aflatoxin B1 (1.25 ppm from 3 to 38 days of age) and ochratoxin A (0.5 ppm from 3 to 38 days of age) along with inclusion body hepatitis virus (IBHV) inoculation (at 10 days of age) singly and in combination was studied in broiler chicks. Birds in combined treatment groups, i.e. aflatoxin fed and virus inoculated and ochratoxin fed and virus inoculated, showed more changes in activities of phosphatases (AKPase, ATPase, G-6-Pase and ACPase) in liver and kidney tissues than their respective individual treatment groups with a few exceptions. Reduction in the activities of oxido-reductases in liver and kidney tissues were almost comparable in different treatment groups. The increase in muco-polysaccharides reaction was more marked in both the combined treatment groups than the single treatment groups. Intensity of lipid reaction was more in ochratoxin virus combination group than either alone.

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Inhibition of the glycogen phosphorylase system during ochratoxicosis in chickens

Cited by 8 publications

References 20 publications

Glycogen storage diseases in animals and their potential value as models of human disease

Glycogen storage diseases in animals and their potential value as models of human disease

Maternal protein deprivation enhances the teratogenicity of ochratoxin a in mice

Histochemical/histoenzymic studies in broiler chicks fed aflatoxin, ochratoxin and inoculated with inclusion body hepatitis virus singly and in concurrence

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