The neurotoxicity of aflatoxin B1 in the rat

Ikegwuonu, Fidelis I.

doi:10.1016/0300-483x(83)90121-x

Cited by 40 publications

(24 citation statements)

References 18 publications

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“…These results are in agreement with previous studies that reported degenerative changes in the rat cerebral cortex and in the cerebellum (Iwanowski, 1988;Ratan et al, 1994). Congestion and dilatation of cerebral, cerebellar and myocardial blood vessels were also reported after chronic exposure to different doses of aflatoxin (Ikegwuonu, 1983;Laag and Abd el Aziz, 2013;Soliman and Tawfik, 2014). The effect on the blood vessels can be attributed to the stimulating effect of aflatoxin on endothelial relaxation factors, such as nitric oxide, (Mannaioni et al, 1997;Wang et al, 2001) and to the toxic effect of AFB1 on the brain microvascular endothelial cells which constitute the blood-brain barrier (Qureshi et al, 2015).…”

Section: Discussionsupporting

confidence: 95%

“…This AFB1-induced cellular degeneration has been attributed to its apoptotic effect in several mammalian tissues, such as kidney and liver (Lei et al, 2013;Liu et al, 2012). AFB1-induced cellular apoptosis was also reported in the central and peripheral nervous system as a result of alterations in the neurochemical levels following repeated administration of aflatoxin (Ikegwuonu, 1983). Similar effect has been also described in vitro, where aflatoxin administration resulted in cellular death of stem cells derived from the neuronal crest (Nones et al, 2012; .…”

Section: Discussionmentioning

confidence: 64%

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Toxic effect of aflatoxin B1 and the role of recovery on the rat cerebral cortex and hippocampus

2015

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Section: Discussionsupporting

confidence: 95%

Section: Discussionmentioning

confidence: 64%

Toxic effect of aflatoxin B1 and the role of recovery on the rat cerebral cortex and hippocampus

2015

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“…This implies that glucose is low, psychological process requiring mental effort may be impaired. The result corroborates the finding of Ikegwuonu (1983) who reported that nerves tissue requirement for glucose molecules were reduced during aflatoxicosis. Glucose has earlier been reported to be the obligatory energy substrate for fuelling brain and it is entirely oxidised to carbon iv oxide and water for optimal use (Magistretti et al, 1999;Kong et al, 2002).…”

Section: Discussionsupporting

confidence: 82%

Acetylcholinesterase, glucose and total protein concenration in the brain regions of West African dwarf goats fed dietary aflatoxin

Ewuola¹,

Bolarinwa²

2017

J. Vet. Med. Anim. Health

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A study was carried out on the effect of varied levels of dietary aflatoxin on acetylcholinesterase, glucose and total protein concentration in the brain regions of West African Dwarf goats. 20 West African Dwarf goats of about 5-6 months old were used for the trial and they were randomly allotted to four dietary treatments containing 0 (control), 50, 100 and 150 µg aflatoxin/kg diet. The animals were housed individually for the feeding trial in a completely randomised designed and the experiment lasted 12 weeks. At the end of the feeding trial, the animals were sacrificed and brain dissected into different regions. The different regions of the brain studied were medulla oblongata, amygdala, hippocampus, cerebral cortex, mid-brain, cerebellum, pons varoli and hypothalamus. Samples were collected from these regions and homogenised to determine acetylcholinesterase, glucose and total protein concentrations. Result showed that the acetylcholinesterase activity in the brain regions was not significantly influenced by the dietary aflatoxin among the treatments. Glucose concentration was significantly (p<0.05) higher in the hypothalamus of animals fed 50 µg aflatoxin/kg and control diet than those fed 100 and 150 µg aflatoxin/kg. Total protein concentration in the medullar oblongata and the hypothalamic regions of the brain in animals fed 150 ppb was significantly (p<0.05) higher than those on the control diet. The pH of the medulla oblongata, amygdala, hippocampus, cerebral cortex were significantly (p<0.05) higher in goats fed 150 mg/kg than those fed the control diet. However, pH was not significant in the mid brain, cerebellum, pons varoli and hypothalamus among the treatments. This study suggests that dietary aflatoxin up to 100 ppb reduced glucose concentration in the hypothalamus and total protein in the medulla oblongata region of the brain with tendency to impair brain function.

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“…Verruculogens and penitrem A may be "tremorgenic mycotoxins," responsible for tremors, ataxia, weakness, and convulsions in animals (392). Unfortunately, studies of many of these toxins were conducted using intraperitoneal injections (45,174,266). Because the route of administration matters greatly and since intraperitoneal injection has no physiologic correlate, the results are of questionable clinical relevance.…”

Section: Neurologicmentioning

confidence: 99%

Indoor Mold, Toxigenic Fungi, andStachybotrys chartarum: Infectious Disease Perspective

2003

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Damp buildings often have a moldy smell or obvious mold growth; some molds are human pathogens. This has caused concern regarding health effects of moldy indoor environments and has resulted in many studies of moisture- and mold-damaged buildings. Recently, there have been reports of severe illness as a result of indoor mold exposure, particularly due to Stachybotrys chartarum. While many authors describe a direct relationship between fungal contamination and illness, close examination of the literature reveals a confusing picture. Here, we review the evidence regarding indoor mold exposure and mycotoxicosis, with an emphasis on S. chartarum. We also examine possible end-organ effects, including pulmonary, immunologic, neurologic, and oncologic disorders. We discuss the Cleveland infant idiopathic pulmonary hemorrhage reports in detail, since they provided important impetus for concerns about Stachybotrys. Some valid concerns exist regarding the relationship between indoor mold exposure and human disease. Review of the literature reveals certain fungus-disease associations in humans, including ergotism (Claviceps species), alimentary toxic aleukia (Fusarium), and liver disease (Aspergillys). While many papers suggest a similar relationship between Stachybotrys and human disease, the studies nearly uniformly suffer from significant methodological flaws, making their findings inconclusive. As a result, we have not found well-substantiated supportive evidence of serious illness due to Stachybotrys exposure in the contemporary environment. To address issues of indoor mold-related illness, there is an urgent need for studies using objective markers of illness, relevant animal models, proper epidemiologic techniques, and examination of confounding factors

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The neurotoxicity of aflatoxin B1 in the rat

Cited by 40 publications

References 18 publications

Toxic effect of aflatoxin B1 and the role of recovery on the rat cerebral cortex and hippocampus

Toxic effect of aflatoxin B1 and the role of recovery on the rat cerebral cortex and hippocampus

Acetylcholinesterase, glucose and total protein concenration in the brain regions of West African dwarf goats fed dietary aflatoxin

Indoor Mold, Toxigenic Fungi, andStachybotrys chartarum: Infectious Disease Perspective

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