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首页> 外文期刊>Archives of Toxicology >Role of high-energy phosphates and their metabolites in protection of carbofuran-induced biochemical changes in diaphragm muscle by memantine.
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Role of high-energy phosphates and their metabolites in protection of carbofuran-induced biochemical changes in diaphragm muscle by memantine.

机译:高能磷酸盐及其代谢产物在美金刚对保护呋喃丹引起的diaphragm肌肌肉生化变化的保护中的作用。

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摘要

A combined antidotal treatment with memantine HCI (MEM, 18 mg/kg, s.c.) and atropine sulfate (ATS, 16 mg/kg, s.c.) provided complete protection against acute carbofuran toxicity (1.5 mg/kg, s.c.) in rats by multiple mechanisms. Carbofuran, in addition to inhibiting serine-containing esterases, also perturbed the activities of mitochondrial/cytoplasmic biomarker enzymes (creatine kinase, CK; and lactic dehydrogenase, LDH) in diaphragm muscle. The observed changes in the activity of biomarker enzymes were reflected in serum as a result of their leakage from the diaphragm due to a depletion of high-energy phosphates, such as adenosine triphosphate (ATP, 27%) and phosphocreatine (PCr, 33%) and their metabolites (ADP, 36%; AMP, 35%; and Cr, 38%). Combined treatment with MEM and ATS provided protection and reversal of the induced changes in biomarkers by preventing depletion of high-energy phosphates and thus maintaining normal cell membrane characteristics, including permeability and integrity. These results, along with those reported previously, indicate that MEM antagonizes carbofuran toxicity by multiple mechanisms.
机译:美金刚盐酸盐(MEM,18 mg / kg,sc)和硫酸阿托品(ATS,16 mg / kg,sc)的联合解毒剂治疗通过多种机制对大鼠的急性呋喃呋喃毒性(1.5 mg / kg,sc)提供了全面的保护。 。除抑制含丝氨酸的酯酶外,呋喃丹还干扰了diaphragm肌中线粒体/细胞质生物标志物酶(肌酸激酶,CK;和乳酸脱氢酶,LDH)的活性。观察到的生物标志物酶活性变化反映在血清中,这是由于高能磷酸盐(例如三磷酸腺苷(ATP,27%)和磷酸肌酸(PCr,33%))的消耗而导致它们从diaphragm膜漏出的结果。及其代谢产物(ADP,36%; AMP,35%; Cr,38%)。 MEM和ATS的联合处理可防止高能磷酸盐的消耗,从而维持正常的细胞膜特性(包括通透性和完整性),从而保护和逆转生物标志物的诱导变化。这些结果以及先前报道的结果表明,MEM通过多种机制拮抗呋喃丹的毒性。

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