ABSTRACT
Neurofilaments [NFs] are the main constitutes of intermediate filaments in neurons. They are composed of three subunits with heavey, medium and low molecular weight. Anti-neurofilament antibodies exist in serum of patients with some neurodegenerative diseases. A fluoroimmunoassay has been developed for determining of antibodies against neurofilaments, using an anti-fluorescein serum and fluorescein-labeled NFs. Antibodies raised against bovine spinal cord NFs in rabbit and the labeled NFs are incubated with anti-fluorescein serum at room temperature. At high levels, binding of anti-neurofilaments [anti-NFs] to labeled NFs prevented subsequent binding of the anti-fluorescein to fluorescein groups, resulting in little change in the signals of the label. Conversely, at low level of anti-NFs the free fraction of the labeled NFs is available to be bound by anti-fluorescein, which markedly reduced fluorescence intensity of label. Thus, the fluorescence intensity of assay mixture directly reflects the amount of anti-NFs antibodies in the serum. It is concluded that the availability of fluorescein-labeled NFs and antibody directed against fluorescein group permit measurement of anti-NFs antibodies in serum of neurodegenerative patients
ABSTRACT
Catecholamine is a group of neurotransmitters that is believed to be responsible for the normal function of animal brain. Physiological and behavioral changes of human body have been reported due to the damage of the brain function following lead exposure. Due to the assumption of lead disposal in brain tissue with two year for its half-life, which results in alteration of brain function, we investigated the ability of lead to change the brain catecholamines during short and long-term studies. Rats were exposed daily with varying amounts of lead and catecholamine contents of cerebellum, mid-brain and brain cortex were determined. Acute peritoneal administration of single dose of lead as lead acetate [260 micro mol/Kg] after 2 h reduced [p < 0.05] the catecholamine levels of cerebellum, mid-brain and cortex part by 34.9%, 35.44% and 23.8%, respectively. The extension of experiment time to 5 h, significant [p < 0.05] reductions in catecholamine levels of mentioned regions of brain by 32.35%, 12.35% and 19.3% were seen respectively. Daily intraperitoneal administration of 10 micro mol/Kg lead for 30 and 60 days reduced catecholamines levels of cerebellum [22.22% and 30.44%], midbrain [12.48% and 26.27%] and brain cortex [11.58% and 26.7%] respectively. It might be concluded that brain dysfunction in lead intoxicated rat occurred through the reduction in the catecholamine levels of different parts of brain. Lead might be therefore considered as a probable factor in causing neurological disease in lead exposed man