The study treated 72 s,rague-Dawley rats that were divided into 4 groups, one controlgroup and low, middle and higa dose groups, through drinking lead acetate solutions for threemonths. On the basis of founding subcl...The study treated 72 s,rague-Dawley rats that were divided into 4 groups, one controlgroup and low, middle and higa dose groups, through drinking lead acetate solutions for threemonths. On the basis of founding subclinical lead poisoning model, behavioral toxicological testwhich consisted of neurobehavioral functions, neuroelectrophysiology and neurobiochemistry wascarried out. The results indicabo that low lvel lead exposure could result in the obvious changes orneurobehavioral function, neuroelectrophyslology and ueurobiochemistry, and the changes of neurobeltavioral runctiou had close correlatiom with P6B, Zap, NCV and DA, and they also had promlnant dose-response relatiouskips. The results suggested that the indexes of neurobehavioral functionmight be cousldered as early, semitive indexes for subolinical'lead poisoning. The combination ofneurobehavioral function with neuroectrophysiology could be used to evaluate the early neurotic toxicity of lead. The results also suggested that the change of dopamine metabolism of the central nervous system (CNS) might be one of the biological foundation of lead neurotic toxicity which changedthe neurobehavioral function of laboratory rats.展开更多
文摘The study treated 72 s,rague-Dawley rats that were divided into 4 groups, one controlgroup and low, middle and higa dose groups, through drinking lead acetate solutions for threemonths. On the basis of founding subclinical lead poisoning model, behavioral toxicological testwhich consisted of neurobehavioral functions, neuroelectrophysiology and neurobiochemistry wascarried out. The results indicabo that low lvel lead exposure could result in the obvious changes orneurobehavioral function, neuroelectrophyslology and ueurobiochemistry, and the changes of neurobeltavioral runctiou had close correlatiom with P6B, Zap, NCV and DA, and they also had promlnant dose-response relatiouskips. The results suggested that the indexes of neurobehavioral functionmight be cousldered as early, semitive indexes for subolinical'lead poisoning. The combination ofneurobehavioral function with neuroectrophysiology could be used to evaluate the early neurotic toxicity of lead. The results also suggested that the change of dopamine metabolism of the central nervous system (CNS) might be one of the biological foundation of lead neurotic toxicity which changedthe neurobehavioral function of laboratory rats.
