Acetamide

[Effect of acetamide on histopathology in cerebral cortex of rats with tetramine poisoning].[Pubmed:24754949]

Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2014 Apr;32(4):289-92.

OBJECTIVE: To observe the effect of different doses of Acetamide on the histopathology in the cerebral cortex of rats with tetramine (TET) poisoning and to provide a basis for the treatment of fluoroAcetamide poisoning with Acetamide. METHODS: Eighty clean Sprague-Dawley rats were randomly divided into five groups: saline control group,dimethylsulfoxide water solution control group,TET poisoning group, Acetamide (2.88 g/kg/d) treatment group, and Acetamide (5.68 g/kg/d) treatment group, with 16 rats in each group. Rats in the poisoning group and treatment groups were poisoned with TET by intragastric administration after fasting; then, saline was injected intramuscularly into rats of the poisoning group, and different doses of Acetamide were injected intramuscularly into rats of treatment groups; the course of treatment was 5 d. At 3 h, 12 h, 48 h, and 7 d after treatment, the cerebral cortex was harvested from rats in each group, and the histopathological changes in the cerebral cortex were evaluated under light and electron microscopes. RESULTS: The light microscopy showed that the TET poisoning group had hypoxia changes in the cerebral cortex, which worsened over time; the treatment groups had reduced hypoxia changes, and the Acetamide (2.88 g/kg/d) treatment group had more reduction than the Acetamide (5.68 g/kg/d) treatment group. The electron microscopy showed that the apoptosis of neuronal cells were the main pathological changes in the TET poisoning group; the treatment groups had reduced apoptotic changes, and the Acetamide (2.88 g/kg/d) treatment group had more reduction than the Acetamide (5.68 g/kg/d) treatment group. CONCLUSION: No pathological changes associated with the synergistic toxic effect of Acetamide and TET are found in the cerebral cortex. Acetamide (2.88 g/kg/d) could reduce central nervous lesions, but the efficacy is not improved after increasing the dose. For patients who cannot be identified with TET or fluoroAcetamide poisoning, Acetamide could be considered for treatment.

[Effects of acetamide at different doses on expression of amino acids in cerebral cortex of rats with acute tetramine poisoning].[Pubmed:25169228]

Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2014 Jun;32(6):438-41.

OBJECTIVE: To investigate the effects of Acetamide at different doses on the expression of inhibitory amino acids (gamma-aminobutyric acid, GABA) and excitatory amino acid (glutamate, Glu) in the cerebral cortex of rats with acute tetramine (TET) poisoning. METHODS: Eighty Sprague-Dawley rats (SPF) were randomly divided into five groups, with 16 rats in each group: saline control group, dimethyl sulfoxide (DMSO) control group, TET exposure group, high-dose (2.8 g/kg/d) Acetamide treatment group, and super-high-dose (5.6 g/kg/d) Acetamide treatment group. Rats in the exposure group and treatment groups were exposed to TET by intragastric administration after fasting, and were then intramuscularly injected with saline or different doses of Acetamide in the following 5 days. The cortex of the temporal lobe was collected at 3 h, 12 h, 48 h, or 7 d after treatment. The expression levels of GABA and Glu in the cortex of the temporal lobe were determined by average optical density (OD) values in immunohistochemistry. RESULTS: 1) Expression of GABA: The OD value of GABA in TET exposure group started to increase at 12 h after treatment, reached the peak at 48 h, and decreased to the normal level at 7 d. In the high-dose Acetamide treatment group, the increase in OD at 12 h was not so significant as that in the TET exposure group, OD value decreased to the normal level at 48 h and was lower than that in the exposure group, and the changes were more like those in the control groups. In the super-high-dose Acetamide treatment group, OD value began to increase significantly at 3 h and was significantly higher than that in the TET exposure group (P < 0.01), it reached the peak at 12 h, and was restored to the normal value at 48 h. 2) Expression of Glu: The OD value of Glu in TET exposure group at 3 h after treatment was significantly lower than those in the two control groups, it increased gradually from 12 h to 48 h, and recovered to the normal level at the 7th d. The changes in the high-dose Acetamide treatment group were similar to those in the TET exposure group, but became more like those in the control groups after 48 h; the OD value in super-high-dose Acetamide treatment group was significantly higher than that in the TET exposure group at 3 h after treatment (P < 0.01), while no significant difference was found at 12 h; it was significantly lower than those of all other groups at 48 h and 7 d (P < 0.01). CONCLUSIONS: Treatment with high dose of Acetamide has some curative effect on TET poisoning-induced central nervous lesion, while the effect of super-high-dose Acetamide on expression of neurotransmitters is too complex to evaluate.