Biochemical and Morphologic Characterization of Acrylamide Peripheral Neuropathy

Lehning, Ellen J.; Persaud, Anita; Dyer, K. R.; Jortner, Bernard S.; LoPachin, Richard M.

doi:10.1006/taap.1998.8464

Cited by 74 publications

(20 citation statements)

References 44 publications

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“…As in previous studies [27], rats sub-chronically exposed to ACR developed changes in body weight and classic signs of ACR behavioral neurotoxicity. Rats dosed with ACR at 50 mg/kg/day showed a progressive and significant decrease in body weight relative to baseline values and a rapid increase in gait score, whereas rats dosed at 21 mg/kg/day produced a retardation of normal weight gaining in body weight and a relatively slow rise in gait score [16].…”

Section: Neurological Status and Body Weight Changesmentioning

confidence: 74%

Acrylamide Alters Cytoskeletal Protein Level in Rat Sciatic Nerves

Sung

Son

et al. 2006

Neurochem Res

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Occupational exposure and experimental intoxication with acrylamide (ACR) produce neuropathy characterized by nerve degeneration. To investigate the mechanism of ACR-induced neuropathy, male adult Wistar rats were given ACR (20, 40 mg/kg i.p. 3 days/week) for 8 weeks. Sciatic nerves were Triton-extracted and centrifuged at a high speed (100,000 x g) to yield pellet and supernatant fractions. The contents of six cytoskeletal proteins (NF-L, NF-M, NF-H, alpha-tubulin, beta-tubulin, and beta-actin) in both fractions were determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting. Results showed that the three neurofilament (NF) subunits (NF-L, NF-M, NF-H) in both the pellet and the supernatant fraction decreased significantly (P < 0.01) in the high-dosing group, except for NF-M in the pellet. alpha-tubulin, beta-tubulin, and beta-actin increased significantly in the supernatant (P < 0.01), whereas both alpha-tubulin and beta-tubulin decreased significantly in the pellet (P < 0.01). However, beta-actin was not altered significantly in the sciatic nerves pellet. These findings suggest that ACR altered the cytoskeletal protein level in sciatic nerve, which may be one of the molecular mechanisms of ACR-induced peripheral neuropathy.

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Section: Neurological Status and Body Weight Changesmentioning

confidence: 74%

Acrylamide Alters Cytoskeletal Protein Level in Rat Sciatic Nerves

Sung

Son

et al. 2006

Neurochem Res

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“…Lehning et al (1998) stated that decreased Na + K + -ATPase activity has been considered as a possible mechanism for peripheral nerve axon damage induced by ACR. Previous reports indicated that Na + K + -ATPase is delivered to axon and nerve terminal sites by a kinesinbased rapid anterograde transport (Lombet et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

Protective role ofPanax ginseng extract standardized with ginsenoside Rg3 against acrylamide-induced neurotoxicity in rats

et al. 2006

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Acrylamide (ACR) is an industrial neurotoxic chemical that has been recently found in carbohydrate-rich foods cooked at high temperatures. ACR was designated as a probable human carcinogen by IARC (1994) and USEPA (1988). Panax ginseng extract has efficacies such as anticancer, antihypertension, antidiabetes and antinociception. The objective of the current study is to evaluate the protective effects of Panax ginseng extract against ACR-induced toxicity in rats. Sixty adult Sprague Dawley female rats were divided into six groups included a control group, a group treated orally with ACR (50 mg kg(-1) body weight; b.w.) for 11 days, a group treated orally with Panax ginseng extract (20 mg kg(-1) b.w.) for 11 days and groups treated orally with Panax ginseng for 11 days before, during or after 11 days of ACR treatment. The results indicated that treatment with ACR alone resulted in a significant increase in lipid peroxidation level and LDH activity in brain homogenate as well as in serum CK activity, whereas it caused a significant decrease in SOD activity and a small but statistically insignificant decrease in Na(+)K(+)-ATPase activity in brain homogenate. Serum serotonin, corticosterone, T3, T4, TSH, estradiol, progesterone and plasma adrenaline were significantly decreased in ACR-treated rats. Treatment with Panax ginseng before, during or after ACR treatment reduced or partially antagonized the effects induced by ACR towards the normal values of controls. It could be concluded that Panax ginseng extract exhibited a protective action against ACR toxicity and it is worth noting that treatment with Panax ginseng extract before or at the same time as ACR treatment was more effective than when administered after ACR treatment.

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“…Their cytoplasm revealed vacuolation and dilated RER. The irregular nuclear outline or the shrinkage of the nucleus might be attributed to neuronal necrosis or DNA damage induced by Bisphenol A [30] . The dilated perinuclar envelop, RER, Golgi and mitochondria can be accounted for by previous reports indicating that oxidative stress by Bisphenol A leads to increased intracellular ROS and oxidative cell damage [14 & 31] .…”

Section: Discussionmentioning

confidence: 99%

Histological study of the possible protective action of omega-3-fatty acids on the injurious effect induced by Bisphenol A on rat hippocampus

Elaziz

Laag

2018

Egyptian Journal of Histology

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Introduction: Bisphenol A (BPA), a well-known industrial chemical, has adverse effects on the brain even at relatively low exposure levels in rodents, primates and humans. Omega-3-fatty acids participate in a number of neuronal processes including neurogenesis, neuron differentiation, and neuro-protection. Aim of the work: To investigate the possible protective action of omega-3-fatty acids on the injurious histological effect induced by Bisphenol A on rat hippocampus. Materials and Methods: Eighteen adult male Wistar rats were divided into 3 equal groups; control, BPA (1.2mg/kg daily for 3 weeks, intraperitoneally) and the third group were given omega-3 (300mg/kg orally) in addition to BPA in the aforementioned dose and duration. Hippocampus sections were processed for hematoxylin and eosin staining, GFAB staining and electron microscopic examination. Results: BBPA administration resulted into several histological alterations. Glial fibrillary acidic protein-positive cells were more abundant in the hippocampus of BPA-treated animals compared with the control animals. Ultra-structurally, the hippocampus of BPA-treated group showed nerve cells having nuclei with irregular outline and dilated perinuclear envelop, dilated RER and Golgi, swollen mitochondria with destroyed cristae. Some of the myelinated and unmyelinated nerve fibers showed degenerative changes. Concomitant administration of omega-3-fatty acids ameliorated these effects. Conclusions: OOmega-3-fatty acids partially minimized the severity of BPA-induced hippocampus injurious histological effects in Wistar rat.

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Biochemical and Morphologic Characterization of Acrylamide Peripheral Neuropathy

Cited by 74 publications

References 44 publications

Acrylamide Alters Cytoskeletal Protein Level in Rat Sciatic Nerves

Acrylamide Alters Cytoskeletal Protein Level in Rat Sciatic Nerves

Protective role ofPanax ginseng extract standardized with ginsenoside Rg3 against acrylamide-induced neurotoxicity in rats

Histological study of the possible protective action of omega-3-fatty acids on the injurious effect induced by Bisphenol A on rat hippocampus

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