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

Bahey, Noha Gamal; Elaziz, Hekmat Osman Abd; Gadalla, Kamal K.E.

doi:10.1016/j.tice.2015.09.001

Cited by 39 publications

(23 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Neuronal loss of fluid content has been previously reported by us in the murine striatum following the same characterized murine model of HUS-encephalopathy [16]. Alternatively, a temporal inhibition in the expressions of NeuN and MBP might have occurred, which recovered after 20 days [29]. These events could occur in those STEC-HUS patients that resolved acute symptoms from neurological disorders [30].…”

Section: Discussionmentioning

confidence: 75%

Shiga toxin 2 from enterohemorrhagic Escherichia coli induces reactive glial cells and neurovascular disarrangements including edema and lipid peroxidation in the murine brain hippocampus

et al. 2019

View full text Add to dashboard Cite

BackgroundShiga toxin 2 from enterohemorrhagic Escherichia coli is the etiologic agent of bloody diarrhea, hemolytic uremic syndrome and derived encephalopathies that may result to death in patients. Being a Gram negative bacterium, lipopolysaccharide is also released. Particularly, the hippocampus has been found affected in patients intoxicated with Shiga toxin 2. In the current work, the deleterious effects of Shiga toxin 2 and lipopolysaccharide are investigated in detail in hippocampal cells for the first time in a translational murine model, providing conclusive evidences on how these toxins may damage in the observed clinic cases.MethodsMale NIH mice (25 g) were injected intravenously with saline solution, lipopolysaccharide, Shiga toxin 2 or a combination of Shiga toxin 2 with lipopolysaccharide. Brain water content assay was made to determine brain edema. Another set of animals were intracardially perfused with a fixative solution and their brains were subjected to immunofluorescence with lectins to determine the microvasculature profile, and anti-GFAP, anti-NeuN, anti-MBP and anti-Iba1 to study reactive astrocytes, neuronal damage, myelin dysarrangements and microglial state respectively. Finally, the Thiobarbituric Acid Reactive Substances Assay was made to determine lipid peroxidation. In all assays, statistical significance was performed using the One-way analysis of variance followed by Bonferroni post hoc test.ResultsSystemic sublethal administration of Shiga toxin 2 increased the expressions of astrocytic GFAP and microglial Iba1, and decreased the expressions of endothelial glycocalyx, NeuN neurons from CA1 pyramidal layer and oligodendrocytic MBP myelin sheath from the fimbria of the hippocampus. In addition, increased interstitial fluids and Thiobarbituric Acid Reactive Substances-derived lipid peroxidation were also found. The observed outcomes were enhanced when sublethal administration of Shiga toxin 2 was co-administered together with lipopolysaccharide.ConclusionSystemic sublethal administration of Shiga toxin 2 produced a deterioration of the cells that integrate the vascular unit displaying astrocytic and microglial reactive profiles, while edema and lipid peroxidation were also observed. The contribution of lipopolysaccharide to pathogenicity caused by Shiga toxin 2 resulted to enhance the observed hippocampal damage.

show abstract

Section: Discussionmentioning

confidence: 75%

Shiga toxin 2 from enterohemorrhagic Escherichia coli induces reactive glial cells and neurovascular disarrangements including edema and lipid peroxidation in the murine brain hippocampus

et al. 2019

View full text Add to dashboard Cite

show abstract

“…[ 16 ] Histopathological lesions associated with AFB 1 exposure include diminution of nerve fibers and neuronal degeneration in the frontal cortex and hippocampus. [ 17 ] Thus, in view of the various harmful impact of AFB 1 on human and animal health, research into the possible antidotes for toxicities due to AFB 1 exposure is warranted.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective role of gallic acid in aflatoxin B₁‐induced behavioral abnormalities in rats

Adedara

Owumi

Oyelere

et al. 2020

J Biochem & Molecular Tox

View full text Add to dashboard Cite

The neurotoxic impact of dietary exposure to aflatoxin B1 (AFB1) is documented in experimental and epidemiological studies. Gallic acid (GA) is a triphenolic phytochemical with potent anticancer, anti‐inflammatory, and antioxidant activities. There is a knowledge gap on the influence of GA on AFB1‐induced neurotoxicity. This study probed the influence of GA on neurobehavioral and biochemical abnormalities in rats orally treated with AFB1 per se (75 µg/kg body weight) or administered together with GA (20 and 40 mg/kg) for 28 uninterrupted days. Behavioral endpoints obtained with video‐tracking software demonstrated significant (p < .05) abatement of AFB1‐induced anxiogenic‐like behaviors (increased freezing, urination, and fecal bolus discharge), motor and locomotor inadequacies, namely increased negative geotaxis and diminished grip strength, absolute turn angle, total time mobile, body rotation, maximum speed, and total distance traveled by GA. The improvement of exploratory behavior in animals that received both AFB1 and GA was confirmed by track plots and heat maps appraisal. Abatement of AFB1‐induced decreases in acetylcholinesterase activity, antioxidant status and glutathione level by GA was accompanied by a marked reduction in oxidative stress markers in the cerebellum and cerebrum of rats. Additionally, GA treatment abrogated AFB1‐mediated decrease in interleukin‐10 and elevation of inflammatory indices, namely tumor necrosis factor‐α, myeloperoxidase activity, interleukin‐1β, and nitric oxide. Further, GA treatment curtailed caspase‐3 activation and histological injuries in the cerebral and cerebellar tissues. In conclusion, abatement of AFB1‐induced neurobehavioral abnormalities by GA involves anti‐inflammatory, antioxidant, and antiapoptotic mechanisms in rats.

show abstract

“…Besides the main mutation of G:C→T:A at TP53 gene, Chawanthayatham et al (2017) found a more heterogeneous set of mutations emerged during a tumor outgrowth induced by AFB1. AFB1 also causes several health problems including gastrointestinal pain, diarrhea, stunted growth, immunosuppressive, and neurotoxic effects in livestock and humans being, as evidenced by several studies ( Bahey et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

The Binding Efficiency and Interaction of Lactobacillus casei Shirota Toward Aflatoxin B1

et al. 2018

View full text Add to dashboard Cite

The use of probiotic as dietary approach to prevent exposure to food contaminant, aflatoxin B1 (AFB1) has greatly increased. Several studies found that AFB1 binding to the bacterial cell wall is strain-specific. Moreover, the interaction between AFB1 and bacterial cell wall is not well-understood, thus warrants further investigation. This research was conducted to assess the ability of Lactobacillus casei Shirota (Lcs) to bind AFB1 at different concentrations and to determine AFB1 binding efficiency of different Lcs cell components including live cell, heat-treated, and cell wall. In addition, the interaction between AFB1 and Lcs was also evaluated via scanning electron microscopy (SEM) and through an animal study. The binding of AFB1 by all Lcs cell components depends on the concentration of available AFB1. Among all Lcs cell components, the live Lcs cells exhibited the highest binding efficiency (98%) toward AFB1. Besides, the SEM micrographs showed that AFB1 induced structural changes on the bacterial cell surface and morphology including rough and irregular surface along with a curve rod-shaped. In vivo experiment revealed that Lcs is capable to neutralize the toxicity of AFB1 on body weight and intestine through the binding process. The animal’s growth was stunted due to AFB1 exposure, however, such effect was significantly (p < 0.05) alleviated by Lcs. This phenomenon can be explained by a significant (p < 0.05) decreased level of blood serum AFB1 by Lcs (49.6 ± 8.05 ng/mL) compared to AFB1-exposed rats without treatment (88.12 ± 10.65 ng/mL). Taken together, this study highlights the potential use of Lcs as a preventive agent against aflatoxicosis via its strong binding capability.

show abstract

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

Cited by 39 publications

References 62 publications

Shiga toxin 2 from enterohemorrhagic Escherichia coli induces reactive glial cells and neurovascular disarrangements including edema and lipid peroxidation in the murine brain hippocampus

Shiga toxin 2 from enterohemorrhagic Escherichia coli induces reactive glial cells and neurovascular disarrangements including edema and lipid peroxidation in the murine brain hippocampus

Neuroprotective role of gallic acid in aflatoxin B₁‐induced behavioral abnormalities in rats

The Binding Efficiency and Interaction of Lactobacillus casei Shirota Toward Aflatoxin B1

Contact Info

Product

Resources

About

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

Cited by 39 publications

References 62 publications

Shiga toxin 2 from enterohemorrhagic Escherichia coli induces reactive glial cells and neurovascular disarrangements including edema and lipid peroxidation in the murine brain hippocampus

Shiga toxin 2 from enterohemorrhagic Escherichia coli induces reactive glial cells and neurovascular disarrangements including edema and lipid peroxidation in the murine brain hippocampus

Neuroprotective role of gallic acid in aflatoxin B1‐induced behavioral abnormalities in rats

The Binding Efficiency and Interaction of Lactobacillus casei Shirota Toward Aflatoxin B1

Contact Info

Product

Resources

About

Neuroprotective role of gallic acid in aflatoxin B₁‐induced behavioral abnormalities in rats