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Coenzyme Q9 (Ubiquinone Q9), the major form of ubiquinone in rodents, is an amphipathic molecular component of the electron transport chain that functions as an endogenous antioxidant. Coenzyme Q9 attenuates the diabetes-induced decreases in antioxidant defense mechanisms. Coenzyme Q9 improves left ventricular performance and reduces myocardial infarct size and cardiomyocyte apoptosis.

Coenzyme Q9 (5 mg/kg; p.o.; once a day for 4 weeks) reduces myocardial ischemia/reperfusion injury.
CoQ₁₀ and CoQ₉ are components of themitochondrial respiratory chain in mammals and can regulate some mitochondrial proteins/functions. Soybean, corn, and rapeseed oils are very rich sources of CoQ₁₀, whereas CoQ₉ has been found in high concentrations in corn oil.
The lack of a functional CoQ₉ protein in homozygous CoQ₉ mutant (CoQ₉(X/X)) mice causes a severe reduction in the CoQ₇ protein and a widespread CoQ deficiency and accumulation of demethoxyubiquinone. The deficit in CoQ induces a brain-specific impairment of mitochondrial bioenergetics performance, a reduction in respiratory control ratio, ATP levels and ATP/ADP ratio and specific loss of respiratory complex I. These effects lead to neuronal death and demyelinization with severe vacuolization and astrogliosis in the brain of CoQ₉ (X/X) mice that consequently die between 3 and 6 months of age.

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