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Acrylamide neurotoxicity on the cerebrum of weaning rats.

Tian SM, Ma YX, Shi J, Lou TY, Liu SS, Li GY - Neural Regen Res (2015)

Bottom Line: Furthermore, biochemical tests in these rats demonstrated that glutamate concentration was significantly reduced, and γ-aminobutyric acid content was significantly increased and was dependent on acrylamide dose.Immunohistochemical staining showed that in the cerebral cortex, γ-aminobutyric acid, glutamic acid decarboxylase and glial fibrillary acidic protein expression increased remarkably in the moderate- and high-dose acrylamide groups.These results indicate that in weaning rats, acrylamide is positively associated with neurotoxicity in a dose-dependent manner, which may correlate with upregulation of γ-aminobutyric acid and subsequent neuronal degeneration after the initial acrylamide exposure.

View Article: PubMed Central - PubMed

Affiliation: School of Basic Medicine, Guangdong Pharmaceutical University, Guangzhou, Guangdong Province, China.

ABSTRACT
The mechanism underlying acrylamide-induced neurotoxicity remains controversial. Previous studies have focused on acrylamide-induced toxicity in adult rodents, but neurotoxicity in weaning rats has not been investigated. To explore the neurotoxic effect of acrylamide on the developing brain, weaning rats were gavaged with 0, 5, 15, and 30 mg/kg acrylamide for 4 consecutive weeks. No obvious neurotoxicity was observed in weaning rats in the low-dose acrylamide group (5 mg/kg). However, rats from the moderate- and high-dose acrylamide groups (15 and 30 mg/kg) had an abnormal gait. Furthermore, biochemical tests in these rats demonstrated that glutamate concentration was significantly reduced, and γ-aminobutyric acid content was significantly increased and was dependent on acrylamide dose. Immunohistochemical staining showed that in the cerebral cortex, γ-aminobutyric acid, glutamic acid decarboxylase and glial fibrillary acidic protein expression increased remarkably in the moderate- and high-dose acrylamide groups. These results indicate that in weaning rats, acrylamide is positively associated with neurotoxicity in a dose-dependent manner, which may correlate with upregulation of γ-aminobutyric acid and subsequent neuronal degeneration after the initial acrylamide exposure.

No MeSH data available.


Related in: MedlinePlus

Neuronal morphology in the cerebral cortex of weaning rats at 4 weeks after acrylamide treatment (hematoxylin-eosin staining).The images show the changes of neurons in the cerebral cortex in the control group (A), low- (B), moderate- (C) and high-dose acrylamide groups (D). Arrows represent abnormal neurons. Scale bar: 25 μm.
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Figure 2: Neuronal morphology in the cerebral cortex of weaning rats at 4 weeks after acrylamide treatment (hematoxylin-eosin staining).The images show the changes of neurons in the cerebral cortex in the control group (A), low- (B), moderate- (C) and high-dose acrylamide groups (D). Arrows represent abnormal neurons. Scale bar: 25 μm.

Mentions: As shown in Figure 2, neurons were in a neat arrangement and the neuronal count did not decrease with administration of acrylamide. However, abnormal neuronal morphology was observed with increased acrylamide dose. Neurons in the moderate-dose acrylamide group showed concentrated nuclei, increased basophilic chromatin and absent nucleoli. Neurons in the high-dose acrylamide group showed increased concentrated nuclei in neurons, darkly-stained basophilic chromatin and small cell bodies.


Acrylamide neurotoxicity on the cerebrum of weaning rats.

Tian SM, Ma YX, Shi J, Lou TY, Liu SS, Li GY - Neural Regen Res (2015)

Neuronal morphology in the cerebral cortex of weaning rats at 4 weeks after acrylamide treatment (hematoxylin-eosin staining).The images show the changes of neurons in the cerebral cortex in the control group (A), low- (B), moderate- (C) and high-dose acrylamide groups (D). Arrows represent abnormal neurons. Scale bar: 25 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4498356&req=5

Figure 2: Neuronal morphology in the cerebral cortex of weaning rats at 4 weeks after acrylamide treatment (hematoxylin-eosin staining).The images show the changes of neurons in the cerebral cortex in the control group (A), low- (B), moderate- (C) and high-dose acrylamide groups (D). Arrows represent abnormal neurons. Scale bar: 25 μm.
Mentions: As shown in Figure 2, neurons were in a neat arrangement and the neuronal count did not decrease with administration of acrylamide. However, abnormal neuronal morphology was observed with increased acrylamide dose. Neurons in the moderate-dose acrylamide group showed concentrated nuclei, increased basophilic chromatin and absent nucleoli. Neurons in the high-dose acrylamide group showed increased concentrated nuclei in neurons, darkly-stained basophilic chromatin and small cell bodies.

Bottom Line: Furthermore, biochemical tests in these rats demonstrated that glutamate concentration was significantly reduced, and γ-aminobutyric acid content was significantly increased and was dependent on acrylamide dose.Immunohistochemical staining showed that in the cerebral cortex, γ-aminobutyric acid, glutamic acid decarboxylase and glial fibrillary acidic protein expression increased remarkably in the moderate- and high-dose acrylamide groups.These results indicate that in weaning rats, acrylamide is positively associated with neurotoxicity in a dose-dependent manner, which may correlate with upregulation of γ-aminobutyric acid and subsequent neuronal degeneration after the initial acrylamide exposure.

View Article: PubMed Central - PubMed

Affiliation: School of Basic Medicine, Guangdong Pharmaceutical University, Guangzhou, Guangdong Province, China.

ABSTRACT
The mechanism underlying acrylamide-induced neurotoxicity remains controversial. Previous studies have focused on acrylamide-induced toxicity in adult rodents, but neurotoxicity in weaning rats has not been investigated. To explore the neurotoxic effect of acrylamide on the developing brain, weaning rats were gavaged with 0, 5, 15, and 30 mg/kg acrylamide for 4 consecutive weeks. No obvious neurotoxicity was observed in weaning rats in the low-dose acrylamide group (5 mg/kg). However, rats from the moderate- and high-dose acrylamide groups (15 and 30 mg/kg) had an abnormal gait. Furthermore, biochemical tests in these rats demonstrated that glutamate concentration was significantly reduced, and γ-aminobutyric acid content was significantly increased and was dependent on acrylamide dose. Immunohistochemical staining showed that in the cerebral cortex, γ-aminobutyric acid, glutamic acid decarboxylase and glial fibrillary acidic protein expression increased remarkably in the moderate- and high-dose acrylamide groups. These results indicate that in weaning rats, acrylamide is positively associated with neurotoxicity in a dose-dependent manner, which may correlate with upregulation of γ-aminobutyric acid and subsequent neuronal degeneration after the initial acrylamide exposure.

No MeSH data available.


Related in: MedlinePlus