An increasingly popular model of Parkinson's disease proposes that the disease is due to a reduced OXPHOS activity caused by damage to Complex I by environmental toxins. This effect is amplified by susceptiblilty to these reagents in some individuals because of mutations/polymorphisms in the mitochondrially encoded subunits of this complex.


Decreased mitochondrial efficiency is known to increase free radical production by mitochondria. This is suggested to increase the levels of oxidation and nitration of proteins, including parkin and the proteosomal proteins which are responsible for removing damaged proteins from the cell.

The result is aggregation of oxidatively-damaged synuclein, a protein prevalent in brain, which then forms so-called Lewy bodies. These aggregates are thought to alter intracellular dynamics and cause apoptotic cell death. In this model, Parkinson's is a systemic disease which progresses fastest in the substantia nigra because of a particularly high rate of free radical production in these dopaminergic cells.

Cat. No.	Name	Reactivity	Amount	Price
MS141	Complex I Enzyme Activity Microplate Assay Kit	human, mouse, rat, bovine	96 tests	$425.00
MS130	Complex I Enzyme Activity Dipstick Assay Kit	human, mouse, rat, bovine	30 tests	$325.00
			90 tests	$595.00

Cat. No.	Name	Reactivity	Amount	Price
MSFX-1	Complex I FlexPlex™ Module	human, bovine	8 tests	$125.00
MS131	Complex I Human Protein Quantity Dipstick Assay Kit	human, bovine	30 tests	$325.00
			90 tests	$595.00
MS133	Complex I Rodent Protein Quantity Dipstick Assay Kit	mouse, rat	30 tests	$325.00
			90 tests	$595.00