Coenzyme Q10 (CoQ10), a lipophilic substituted benzoquinone, is present in animal and plant cells. It is endogenously synthetized in every cell and involved in a variety of cellular processes. CoQ10 is an obligatory component of the respiratory chain in inner mitochondrial membrane. In addition, the presence of CoQ10 in all cellular membranes and in blood. It is the only endogenous lipid antioxidant. Moreover, it is an essential factor for uncoupling protein and controls the permeability transition pore in mitochondria. It also participates in extramitochondrial electron transport and controls membrane physicochemical properties. CoQ10 effects on gene expression might affect the overall metabolism. Primary changes in the energetic and antioxidant functions can explain its remedial effects. CoQ10 supplementation is safe and well-tolerated, even at high doses. CoQ10 does not cause any serious adverse effects in humans or experimental animals. New preparations of CoQ10 that are less hydrophobic and structural derivatives, like idebenone and MitoQ, are being developed to increase absorption and tissue distribution. The review aims to summarize clinical and experimental effects of CoQ10 supplementations in some neurological diseases such as migraine, Parkinson ́s disease, Huntington ́s disease, Alzheimer ́s disease, amyotrophic lateral sclerosis, Friedreich ́s ataxia or multiple sclerosis. Cardiovascular hypertension was included because of its central mechanisms controlling blood pressure in the brainstem rostral ventrolateral medulla and hypothalamic paraventricular nucleus. In conclusion, it seems reasonable to recommend CoQ10 as adjunct to conventional therapy in some cases. However, sometimes CoQ10 supplementations are more efficient in animal models of diseases than in human patients (e.g. Parkinson ́s disease) or rather vague (e.g. Friedreich ́s ataxia or amyotrophic lateral sclerosis).
- MeSH
- Antioxidants pharmacology MeSH
- Humans MeSH
- Mitochondrial Diseases * metabolism MeSH
- Mitochondria metabolism MeSH
- Nervous System Diseases * drug therapy metabolism MeSH
- Electron Transport MeSH
- Ubiquinone analogs & derivatives therapeutic use MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
Epidemiological studies have demonstrated that n-3 polyunsaturated fatty acid (PUFA) consumption is associated with a reduced risk of atherosclerosis and hyperlipidemia. It is well known that lipid metabolism is also influenced by thyroid hormones. The aim of our study was to test whether n-3 PUFA supplementation (200 mg/kg of body weight/day for 6 weeks given intragastrically) would affect lipid metabolism in Lewis male rats with altered thyroid status. Euthyroid, hypothyroid, and hyperthyroid status of experimental groups was well defined by plasma levels of triiodothyronine, the activity of liver mitochondrial glycerol-3-phosphate dehydrogenase, and by relative heart weight. Fasting blood glucose levels were significantly higher in the hyperthyroid compared to the euthyroid and hypothyroid rats (5.0±0.2 vs. 3.7±0.4 and 4.4±0.2 mmol/l, respectively). In hyperthyroid animals, the concentration of plasma postprandial triglycerides was also increased compared to euthyroid and hypothyroid rats (0.9±0.1 vs. 0.5±0.1 and 0.4±0.1 mmol/l, respectively). On the other hand, hypothyroidism compared to euthyroid and hyperthyroid status was associated with elevated plasma levels of total cholesterol (2.6±0.2 vs. 1.5±0.1 and 1.6±0.1 mmol/l, respectively), LDL cholesterol (0.9±0.1 vs. 0.4±0.1 and 0.2±0.1 mmol/l, respectively) as well as HDL cholesterol (1.6±0.1 vs. 1.0±0.1 and 1.3±0.1 mmol/l, respectively). Supplementation of n-3 PUFA in the present study did not significantly modify either relative heart weight or glucose and lipid levels in any thyroid status.
- MeSH
- Cholesterol metabolism MeSH
- Glycerolphosphate Dehydrogenase metabolism MeSH
- Thyroid Hormones metabolism MeSH
- Hyperthyroidism enzymology metabolism MeSH
- Hypothyroidism enzymology metabolism MeSH
- Liver metabolism MeSH
- Rats MeSH
- Fatty Acids, Omega-3 administration & dosage metabolism MeSH
- Humans MeSH
- Lipid Metabolism * MeSH
- Mitochondria enzymology metabolism MeSH
- Rats, Inbred Lew MeSH
- Dietary Supplements analysis MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Humans MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
AIM: It is well-known that salt hypertension is associated with increased oxidative stress. Since the development of salt hypertension is age-dependent, we were interested whether young and adult salt hypertensive Dahl rats differ in oxidative stress level and/or in the effects of chronic antioxidant therapy on blood pressure (BP) level and on the participation of particular vasoconstrictor/vasodilator systems in BP maintenance. METHODS: Young (5-week-old) and adult (12-week-old) salt-sensitive (Dahl-S) male rats were fed high-salt diet (5% NaCl) and drank tempol solution (2 mm) for 5 weeks. BP was monitored with radiotelemetry and vasoconstrictor/vasodilator balance was evaluated at the end of experiment. Moreover, NO synthase activity, superoxide production and lipoperoxidation were determined in heart, kidney and aorta in separate subgroups of Dahl rats. RESULTS: Tempol treatment had quite opposite BP effects in young and adult Dahl-S rats. While it tended to increase BP in young salt hypertensive Dahl-S rats, it significantly lowered BP in the adult ones due to reduced sympathetic vasoconstriction. Importantly, high salt intake substantially reduced NO synthase activity in heart and kidney, and markedly increased superoxide production in kidneys and aorta of adult Dahl-S rats in which BP correlated positively with superoxide production in thoracic aorta and lipoperoxidation in kidneys. CONCLUSION: Chronic antioxidant therapy lowered BP only in adult salt hypertensive Dahl-S rats in which superoxide levels were increased in both kidneys and aorta. Blood pressure reduction induced by chronic tempol treatment is related to attenuated sympathetic vasoconstriction rather than to augmented NO-dependent vasodilatation.
- MeSH
- Antioxidants administration & dosage pharmacology MeSH
- Sodium Chloride adverse effects MeSH
- Cyclic N-Oxides administration & dosage pharmacology MeSH
- Hypertension drug therapy MeSH
- Blood Pressure drug effects MeSH
- Rats MeSH
- Oxidative Stress drug effects MeSH
- Rats, Inbred Dahl MeSH
- Spin Labels MeSH
- Aging MeSH
- Sympathetic Nervous System MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
