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April 2003

Coenzyme Q10

Neuronal death in the rat hippocampus in experimental diabetes and cerebral ischaemia treated with antioxidants.

Male Wistar rats were subjected to intraperitoneal (i.p.) streptozotocin (STZ) administration (85 mg/kg) to evoke diabetes. Cerebral ischaemia was produced by injection of 0.03 ml of air into the left carotid followed by bilateral common carotid ligation. We studied the effect of application of two antioxidants-coenzyme Q10 (CoQ10, 10 mg/kg b.w., i.p. for seven days) and lipoic acid (LA, 100 mg/kg b.w., i.p. for seven days) on neurones and on the apoptosis-related enzyme-caspase-3 activity in the hippocampus and dentate gyrus. Ischaemia and diabetes lead to a decrease of nuclear and perikaryon diameters as well as neuronal density in the CA1, CA2, CA3 and dentate gyrus. Application of CoQ10 or LA for seven days improved the mean nucleus area and perikaryon area in almost all investigated structures. Both antioxidants diminished neuronal loss in the diabetes complicated with ischaemia but not in the animals with diabetes only. Activity of one of the key enzymes in apoptotic cell death, caspase-3 (CPP32), increased in hippocampus in the diabetic rats, in the animals with cerebral ischaemia and in the rats with both diabetes and ischaemia by about 80%, 33% and 53%, respectively. Either the CoQ10 or the LA treatment led to a significant decrease of the CPP32 activity in all experimental groups. Our results confirm the presence of neuronal damage and death in the hippocampus and dentate gyrus in the experimental STZ-diabetes and its aggravation by the additional cerebral ischaemia. The effects of the antioxidative treatment support the hypothesis of an important role of oxidative stress and free radicals in neuronal pathology in diabetes and ischaemia. The above results of CPP32 activity suggest an important role of apoptosis as a mechanism of cell death and demonstrate the positive effect of the CoQ10 and the LA treatment.

Folia Neuropathol 2001;39(3):147-54

Ubiquinone (coenzyme q10) and mitochondria in oxidative stress of Parkinson's disease.

Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease affecting approximately 1% of the population older than 50 years. There is a worldwide increase in disease prevalence due to the increasing age of human populations. A definitive neuropathological diagnosis of Parkinson's disease requires loss of dopaminergic neurons in the substantia nigra and related brain stem nuclei, and the presence of Lewy bodies in remaining nerve cells. The contribution of genetic factors to the pathogenesis of Parkinson's disease is increasingly being recognized. A point mutation which is sufficient to cause a rare autosomal dominant form of the disorder has been recently identified in the alpha-synuclein gene on chromosome 4 in the much more common sporadic, or 'idiopathic' form of Parkinson's disease, and a defect of complex I of the mitochondrial respiratory chain was confirmed at the biochemical level. Disease specificity of this defect has been demonstrated for the parkinsonian substantia nigra. These findings and the observation that the neurotoxin 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP), which causes a Parkinson-like syndrome in humans, acts via inhibition of complex I have triggered research interest in the mitochondrial genetics of Parkinson's disease. Oxidative phosphorylation consists of five protein-lipid enzyme complexes located in the mitochondrial inner membrane that contain flavins (FMN, FAD), quinoid compounds (coenzyme Q10, CoQ10) and transition metal compounds (iron-sulfur clusters, hemes, protein-bound copper). These enzymes are designated complex I (NADH:ubiquinone oxidoreductase, EC 1.6. 5.3), complex II (succinate:ubiquinone oxidoreductase, EC, complex III (ubiquinol:ferrocytochrome c oxidoreductase, EC, complex IV (ferrocytochrome c:oxygen oxidoreductase or cytochrome c oxidase, EC, and complex V (ATP synthase, EC A defect in mitochondrial oxidative phosphorylation, in terms of a reduction in the activity of NADH CoQ reductase (complex I) has been reported in the striatum of patients with Parkinson's disease. The reduction in the activity of complex I is found in the substantia nigra, but not in other areas of the brain, such as globus pallidus or cerebral cortex. Therefore, the specificity of mitochondrial impairment may play a role in the degeneration of nigrostriatal dopaminergic neurons. This view is supported by the fact that MPTP generating 1-methyl-4-phenylpyridine (MPP(+)) destroys dopaminergic neurons in the substantia nigra. Although the serum levels of CoQ10 is normal in patients with Parkinson's disease, CoQ10 is able to attenuate the MPTP-induced loss of striatal dopaminergic neurons.

Biol Signals Recept 2001 May-Aug;10(3-4):224-53

Vitamin D

A cost-effectiveness analysis of calcium and vitamin D supplementation, etidronate and alendronate in the prevention of vertebral fractures in women treated with glucocorticoids.

OBJECTIVE: To assess the relative costs and benefits of calcium and vitamin D supplements, cyclic etidronate or alendronate in the prevention of vertebral fractures for women with normal bone density and osteopenia who are about to initiate moderate dose glucocorticoid treatment. METHODS: Using a decision analysis model, we evaluated the following patients: four hypothetical cohorts: 30-yr-old women with normal lumbar spine (LS) bone mineral density (BMD) (t score = 0), 50-yr-old women with borderline osteopenia (t score = -1), 60-yr-old women with moderate osteopenia (t score = -1.5) and 70-yr-old women with severe osteopenia (t score = -2) treated with a mean prednisone dose of 10 mg/day for one year. The main outcomes included the development of vertebral fractures 10-years after glucocorticoid treatment and at age 80 (life-time risk) and direct and indirect costs. RESULTS: At 10 years, calcium and vitamin D supplements decreased fracture rates by 30% to 50% at a minimal cost (US$800 or less per vertebral fracture avoided) or at a cost saving compared to no treatment for women with osteopenia (t score -1 to -2). Etidronate and alendronate are most cost-effective in women with borderline osteoporosis (t scores of -1.5 and -2) in the 10 year analysis. In the lifetime analysis, calcium and vitamin D treatment yielded a cost savings compared to no treatment for all groups with osteopenia. Etidronate decreased fracture rates further in all groups at a cost of less than $2,000 per fracture prevented. Alendronate reduced the fracture risk further at cost of $3,000 to $7,000 per fracture avoided. CONCLUSION: Calcium and vitamin D supplements and low cost bisphosphonate regimens such as cyclic etidronate decrease the lifetime vertebral fracture risk at acceptable costs and should be considered when initiating glucocorticoid treatment for women who do not have osteoporosis.

J Rheumatol 2003 Jan;30(1):132-8

A rationale for vitamin D prescribing in a falls clinic population.

OBJECTIVE: To assess the prevalence of vitamin D insufficiency in a falls clinic population. To identify simple clinical predictors of vitamin D insufficiency. DESIGN: Prospective observational descriptive study. PARTICIPANTS: 400 consecutive patients who attended a falls clinic taking referrals from a casualty department or general practitioners. RESULTS: Hypovitaminosis D is very common, affecting at least 72% of a falls clinic population. The number of times an individual goes out per week and serum albumin are independent predictors of hypovitaminosis D, but the predictive value is low. CONCLUSIONS: The prevalence of vitamin D insufficiency is high in a falls clinic population. It is difficult to predict which individuals are most at risk within this population. The benefits of vitamin D supplementation in older people are well recognized. Therefore in the absence of toxic effects, a pragmatic approach may be to supplement all attendees at a falls clinic.

Age Ageing 2002 Jul;31(4):267-71


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