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| The neurobehavioral toxicity and biochemical mechanism of semicarbazide in rats |
| HE Yong-jian1, LIU Rui-jing1, LIU Huan1, ZHENG Dong-dong1, WANG He-wei1, ZHOU Xiong1, LIU Chun-hong1,2 |
1. Food College, South China Agricultural University, Guangzhou 510624, China;
2. Guangdong Provincial Key Laboratory of Food Quality and Safety, Guangzhou 510642, China |
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Abstract To study the neurobehavioral toxicity of semicarbazide (SEM) in rats and its biochemical mechanism. A total of 44male SD rats were randomly divided into 4groups (n=11 per group):control group, low-dose group, medium-dose group, and high-dose group. SEM was intragastrically administrates at the dosage of 0, 7.5, 15, 30mg/kg (body weight) for 28days. The open field test (OFT) and elevated plus maze (EPM) were used to evaluated the neurobehavior in rats before and after exposure to SEM. The gamma-aminobutyric acid (GABA) and glutamate acid (GLU) of hippocampus were determined by liquid chromatography. ELISA method was used to mesure the contents of 5-hydroxytryptamine (5-HT), norepinephrine (NE), dopamine (DA), monoamine oxidase (MAO) and N-methyl-d-aspartic acid receptor (NMDAR). The results showed that the total distance traveled and the distance traveled in the center were significantly lower in the high-dose SEM group compared with the control group (P<0.05). The open arm time percentage and open arm entries percentage were significantly lower in the SEM groups than in the control group (P<0.05 or P<0.01). Compared with the control group, the concentrations of GABA and the activity of MAO were decreased, whereas the levels of GLU, NMDAR, 5-HT, NE and DA were increased in different exposed groups. SEM might affect the nervous system of rats by damaging the mutual transformation of GABA and GLU, increasing the concentration of NMDAR and inhibiting the activity of MAO that directly enhance the levels of monoamine neurotransmitters.
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Received: 02 May 2018
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