Cellometer used in study to examine secondary effects of MAO inhibitors

In the “catecholaldehyde hypothesis” of Parkinson’s disease neurodegeneration, cytoplasmic dopamine (DA) is converted to 3,4-dihydroxyphenylacetaldehyde (DOPAL) by the enzyme monoamine oxidase-A (MAO-A). DOPAL is a toxic substance, generating free radicals and inhibiting mitochondrial function. Scientists at NIH wanted to compare the abilities of currently available MAO-A and MAO-B inhibiting drugs at decreasing endogenous DOPAL levels. Using PC12 cells, six drugs were tested for their effects on DOPAL: MAO-A inhibitor clorygyline, three reversible MAO-A inhibitors, and the MAO-B inhibitors selegiline and rasagiline. The Cellometer was used to count the cells throughout experimentation. Clorgyline, rasagiline, and selegiline decreased DOPAL levels in both [...]

By |2015-12-22T11:52:59+00:00December 22nd, 2015|Categories: Cellometer User Publications|Tags: , , , |0 Comments

Cellometer participates in study to ascertain rotenone mechanism of action

A common hypothesis concerning the pathogenesis of Parkinson’s neurodegeneration suggests that cytoplasmic dopamine (DA) is converted to the auto-toxic 3,4-dihydroxyphenylacetaldehyde (DOPAL), which is neutralized by aldehyde dehydrogenase (ALDH). NIH researchers studied whether rotenone, a substance typically used to create in vitro models of Parkinson neurodegeneration, inhibits ALDH function. PC12 cells were exposed to various concentrations of rotenone in the presence or absence of F-dopamine. Catecholamine metabolism was then measured. The Cellometer maintained cell counts throughout experimentation. Rotenone increased DOPAL while decreasing dopamine levels in cell culture, but in a test tube, the DOPAL to DOPAC conversion by ALDH was not [...]

By |2015-12-15T10:00:57+00:00December 15th, 2015|Categories: Cellometer User Publications|Tags: , , |0 Comments