Limits...
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

GABA-immunoreactive neurons in cerebral cortex at 4 weeks after acrylamide treatment.The images show the immunoreactivity of GABA in the cerebral cortex in the control (A), low- (B), moderate- (C), and high-dose acrylamide groups (D). Scale bar: 25 μm. (E) Densitometry of GABA immunoreactivity. Data are expressed as the mean ± SD (n = 6). The differences between groups were compared with one-way analysis of variance, followed by Dunnett's post hoc test. *P < 0.05, vs. I (0 mg/kg); #P < 0.05, vs. II (5 mg/kg); &P < 0.05, vs. III (15 mg/kg). GABA: Gamma aminobutyric acid; I: control group; II: low-dose acrylamide group (5 mg/kg); III: moderate-dose acrylamide group (15 mg/kg); IV: high-dose acrylamide group (30 mg/kg).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4498356&req=5

Figure 4: GABA-immunoreactive neurons in cerebral cortex at 4 weeks after acrylamide treatment.The images show the immunoreactivity of GABA in the cerebral cortex in the control (A), low- (B), moderate- (C), and high-dose acrylamide groups (D). Scale bar: 25 μm. (E) Densitometry of GABA immunoreactivity. Data are expressed as the mean ± SD (n = 6). The differences between groups were compared with one-way analysis of variance, followed by Dunnett's post hoc test. *P < 0.05, vs. I (0 mg/kg); #P < 0.05, vs. II (5 mg/kg); &P < 0.05, vs. III (15 mg/kg). GABA: Gamma aminobutyric acid; I: control group; II: low-dose acrylamide group (5 mg/kg); III: moderate-dose acrylamide group (15 mg/kg); IV: high-dose acrylamide group (30 mg/kg).

Mentions: GABA-immunoreactive substances were brown and round and distributed in the cytoplasm of neurons. GABA-immunoreactive neurons were spread widely in the cerebral cortex. Rats from the low-dose acrylamide group showed light GABA staining in neurons. Rats from the moderate- and high-dose acrylamide groups displayed intense GABA staining. GABA-immunoreactive neurons from all groups did not exhibit obvious morphological changes (Figure 4). Quantitative analysis showed that the mean optical density of GABA-immunoreactive neurons in moderate- and high-dose acrylamide groups increased significantly (P < 0.05) when compared with the control group (Figure 4).


Acrylamide neurotoxicity on the cerebrum of weaning rats.

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

GABA-immunoreactive neurons in cerebral cortex at 4 weeks after acrylamide treatment.The images show the immunoreactivity of GABA in the cerebral cortex in the control (A), low- (B), moderate- (C), and high-dose acrylamide groups (D). Scale bar: 25 μm. (E) Densitometry of GABA immunoreactivity. Data are expressed as the mean ± SD (n = 6). The differences between groups were compared with one-way analysis of variance, followed by Dunnett's post hoc test. *P < 0.05, vs. I (0 mg/kg); #P < 0.05, vs. II (5 mg/kg); &P < 0.05, vs. III (15 mg/kg). GABA: Gamma aminobutyric acid; I: control group; II: low-dose acrylamide group (5 mg/kg); III: moderate-dose acrylamide group (15 mg/kg); IV: high-dose acrylamide group (30 mg/kg).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 4: GABA-immunoreactive neurons in cerebral cortex at 4 weeks after acrylamide treatment.The images show the immunoreactivity of GABA in the cerebral cortex in the control (A), low- (B), moderate- (C), and high-dose acrylamide groups (D). Scale bar: 25 μm. (E) Densitometry of GABA immunoreactivity. Data are expressed as the mean ± SD (n = 6). The differences between groups were compared with one-way analysis of variance, followed by Dunnett's post hoc test. *P < 0.05, vs. I (0 mg/kg); #P < 0.05, vs. II (5 mg/kg); &P < 0.05, vs. III (15 mg/kg). GABA: Gamma aminobutyric acid; I: control group; II: low-dose acrylamide group (5 mg/kg); III: moderate-dose acrylamide group (15 mg/kg); IV: high-dose acrylamide group (30 mg/kg).
Mentions: GABA-immunoreactive substances were brown and round and distributed in the cytoplasm of neurons. GABA-immunoreactive neurons were spread widely in the cerebral cortex. Rats from the low-dose acrylamide group showed light GABA staining in neurons. Rats from the moderate- and high-dose acrylamide groups displayed intense GABA staining. GABA-immunoreactive neurons from all groups did not exhibit obvious morphological changes (Figure 4). Quantitative analysis showed that the mean optical density of GABA-immunoreactive neurons in moderate- and high-dose acrylamide groups increased significantly (P < 0.05) when compared with the control group (Figure 4).

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