Neurochemical Mechanisms in Disease P14 pdf

Vitamin Deficiencies 115 (Gibson and Blass, 1985). Also, antiniacin compounds can induce deficiency states within days in rodents on a normal diet. Neurological symptoms are more obvious in rats with antimetabolite-induced niacin deficiencies than in the corn-fed dogs. Niacin deficiency causes pellagra which includes mental symptoms and was once common in areas where American corn was a dietary staple. Addition of purified niacin to t he diet has largely abolished the disorder. Pellagra is associated with the “four Ds”: dermatitis, diarrhea, dementia, and death. Dietary niacin deficiency reduces the levels of NAD and NADP coenzymes in the brain. Niacin requirements can be modified by genetic and environmental factors. Hartnup syndrome is a hereditary disorder in which tryptophan transport is impaired and niacin requirements increase. A chronic toxic delirium may be the only clinical abnormal- ity, at least early in the course of the disorder. The delirium may resemble some forms of schizophrenia (Gibson and Blass, 1985). Neuropathological changes seen in pellagra are restricted to neurons and the characteristic finding is chromatolysis. Affected neurons are ballooned, there is loss of Nissl substance, and the nuclei are located eccentrically. Although the issue of chromatolysis has been debated (Harper and Butterworth, 1997) the consensus now is that the brain regions and lesion characteristics are a function of the nature of the underlying cause (dietary, alcohol-related, or isoniazid toxicity). At present, pellagra is encountered most often in patients with chronic alco- holism, often referred to as alcoholic pellagra encephalopathy (APE). APE patients often show only disturbances of consciousness, but may also manifest myoclonus and ataxia. Administration of niacin is recommended in APE patients showing myoclonus and ataxia even without the classical symptoms found in endemic pellagra patients (Sakai et al., 2006). Epidemiological studies suggest that niacin may be implicated in the pathogen- esis of Parkinson’s disease via the following process. NAD produced from niacin releases nicotinamide via poly(ADP-ribosyl)ation which is activated in Parkinson’s disease. Released excess nicotinamide is methylated to 1-methylnicotinamide (MNA) in the cytoplasm by nicotinamide N-methyltransferase. MNA destroys several subunits of complex I via superoxide formation. This can destroy complex I subunits either directly or indirectly via mitochondrial DNA damage, and stimulates poly(ADP-ribosyl)ation. It has been proposed that this implicates nicotinamide as a potential causal agent in the development of Parkinson’s disease (Fukushima et al., 2004). 6 Folic Acid (Vitamin B 9 ) Folate (pteroylglutamic acid) is essential for the synthesis and methylation of DNA during fetal and early postnatal development (Nunn et al., 1986). Folate deficiency may result from poor diet, malabsorption, from treatment with anticonvulsant drugs such as phenytoin or primidone, as well as from antifolate drugs such as methotrexate. Folate deficiency during pregnancy leads to an increased prevalence of fetal malformations such as spina bifida and related neural tube defects. Findings 116 C. Bémeur et al. from two multicentre trials confirmed that folate supplements starting periconcep- tionally and continuing through pregnancy reduce the risk of neural tube defects (Werler et al., 1993; MRC Vitamin Study, 1991). Studies in experimental animals suggest that folate deficiency during gestation and lactation results in alterations of myelin lipids (Hirono and Wada, 1978). Studies in the developing rat central nervous system suggest that folate uptake and storage depend upon a folate-binding protein (10-formyltetrahydrofolate dehydrogenase) which is preferentially localized in glial cells (Martinasevic et al., 1999). 7 Antioxidant Vitamins Oxidative stress has been clearly implicated in a wide range of human diseases by an impressive body of scientific evidence. Oxidative stress is an imbalance in the equi- librium status of pro-oxidant/antioxidant systems in cells (Sies, 1985) and comes from external sources such as ionizing radiation, toxins, drugs, chemicals and environmental pollutants, or endogenous sources resulting from (patho)physiological metabolism of the cell. Antioxidant compounds can be classified into several gen- eral categories: (1) antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, catalase, and heme-oxygenase, (2) antioxidants s uch as vitamin E (α- tocopherol), vitamin C (ascorbic acid), and carotenoids, (3) secondary antioxidants including selenium, zinc, riboflavin, and manganese and, finally, (4) antioxidants such as flavonoids, coenzyme Q, lipoic acid, albumin, and bilirubin. Deficiency of any antioxidant vitamin or nutrient has the potential to lead to an imbalance which may to cause oxidative stress. 7.1 α-Tocopherol (Vitamin E) α-Tocopherol is a lipid-soluble vitamin which is an effective antioxidant. Vitamin E consists of two groups of lipid-soluble compounds: tocopherol and tocotrienol. In humans, α-tocopherol predominates and is considered the more active form of the vitamin. Vitamin E was first isolated as a factor that prevented infertility in rats (Evans and Bishop, 1922). It can inhibit the peroxidation of polyunsaturated fatty acids and it stimulates prostacyclin synthesis which promotes vasodilation and platelet aggregation. Vitamin E also protects membrane structure. Vitamin E deficiency is quite rare. Nevertheless, pure vitamin E deficiency secondary to deficiencies in absorption have been described (Traber, 2006). Vitamin E deficiency can occur with abetalipoproteinemia, cholestatic liver disease, fat malabsorption, celiac disease, cystic fibrosis, and small bowel resection. The typical neurological syndrome in humans is a spinocerebellar degeneration, with loss of reflexes, ataxia, and impaired vibration and position sense. A severe and chronic deficiency of vitamin E is associated with a characteristic neurological syndrome with typical clinical, neuropathological, and electrophysiological abnormalities in both humans and experimental animals. Chronic vitamin E Vitamin Deficiencies 117 deficiency (38 weeks) in mice decreases superoxide radical production in multiple regions of male brain (Cuddihy et al., 2004). These results suggest that α-tocopherol can act as a nonclassic uncoupler. Significant impairment in neural and visual function are observed in vitamin E-deficient rats after approximately 8 months (Hayton and Muller, 2004). Low serum vitamin E is associated with demyelinating motor– sensory neuropathy related to spinocerebellar ataxia (Puri et al., 2005). Vitamin E supplementation leads to clinical and electrophysiological recovery of sensory conduction and evoked potentials; motor nerve conduction, however, shows only partial recovery. Vitamin E deficiency has also been associated with an increase in lipid peroxidation and protein oxidation in the rat brain (Jolitha et al., 2006). The concentration of free malondialdehyde (an indicator of lipid peroxidation) is significantly increased in tissues from vitamin E-deficient compared to control animals. This is consistent with a deficiency of α-tocopherol causing increased lipid peroxidation leading to abnormal neural electrophysiology (Hayton and Muller, 2004). A longitudinal study recently showed significant improvements in growth and a number of electrophysiological parameters of both neural and visual function after repletion with vitamin E (Hayton et al., 2006). It was suggested that vitamin E could play a role in hypothalamo–pituitary system regulation. Early vitamin E supplementation may provide considerable improvement of neurological signs and other associated abnormalities (Marzouki et al., 2005). A wide range of cell culture, animal, and human epidemiological studies are suggestive of a role of vitamin E in brain function and in the prevention of neurodegeneration. It was recently suggested that vitamin E deficiency results in transcriptional alterations in the cerebral cortex of the rat which are consistent with the observed neurological and electrophysiological alterations (Hyland et al., 2006). Vitamin E deficiency was shown to have a strong impact on gene expression in the hippocampus. An important number of genes found to be regulated by vitamin E are associated with hormones and hormone metabolism, and clearance of amyloid-beta and advanced glycated end-products. A protective effect of vitamin E in AD pro- gression has been reported (Rota et al., 2005). A recent study strongly supports the hypothesis of an impairment of lipophilic antioxidant delivery to neuronal cells in AD which could facilitate oxidative stress (Mas et al., 2006). Low-plasma vitamin E concentrations may represent a higher risk of developing dementia in subsequent years (Helmer et al., 2003). The retention and secretion of vitamin E are regulated by α-tocopherol trans- fer protein (αTP) in the brain. Dysfunction of αTP results in deficiency of vitamin E in humans and mice, and increased oxidative stress i n mouse brain. Ataxia with isolated vitamin E deficiency (AVED) is an autosomal recessive neurode- generative disorder due to mutations in the αTP protein gene on chromosome 8q13. This genetic disorder is characterized by neurological symptoms often with a striking resemblance to those of Friedrich’s ataxia. AVED patients have progressive spinocerebellar symptoms and markedly reduced plasma levels of vitamin E (Mariotti et al., 2004). Vitamin E supplementation therapy allows 118 C. Bémeur et al. stabilization of the neurological conditions in most of the patients. However, development of spasticity and retinitis pigmentosa can appear during therapy (Mariotti et al., 2004). 7.2 Ascorbic Acid (Vitamin C) Vitamin C is used as the generic descriptor for all compounds exhibiting quali- tatively the biological activity of ascorbic acid. Ascorbic acid is an unsaturated sugar derivative that is a potent reducing agent. The oxidation of ascorbic acid to dehydroascorbic acid is reversible (Fig. 7). Both forms are biologically active. Because dehydroascorbic acid is readily reduced in vivo, it possesses vitamin C (anti-scurvy) activity, whereas diketogulonic acid, a metabolite, has no activity. Vitamin C has many functions in the organism, not least of which is the absorption and metabolism of iron. It is an effective antioxidant. Ascorbic acid participates in neurotransmitter synthesis as well as the synthesis of collagen. Vitamin C is neces- sary for the synthesis of carnitine and facilitates immune functions. Finally, ascorbic acid participates in the hydroxylation of catecholamines. The uptake of ascorbic acid into synaptosomes requires glucose and oxygen; uptake into the brain appears to be via the cerebrospinal fluid rather than the blood. Fatigue and emotional changes are common in the full-blown deficiency disease scurvy, but diffuse disease of the small blood vessels with small haemorrhages is much more striking. Ascorbic acid has been implicated in many neurological diseases. There is a strong inverse relation between serum vitamin C concentration and stroke incidence CH 2 OH H 2 O HO CH 2 OH CHHOCH OO OO OO O O diketogulon acid oxalic and threonic acids and other products dehydroascorbic acidascorbic acid C C OH OH 2H + 2e – 1H + 1e – OH 4 3 2 1 4 3 2 1 1 2 O C HC OH HO CH CH 2 OH 3 4 Fig. 7 Structure of a scorbic acid (vitamin C). Oxidation of ascorbic acid to dehydrogenase acid is reversible; both forms are biologically active Vitamin Deficiencies 119 (Sanchez-Moreno et al., 2004). Epidemiological evidence links adequate vitamin C ingestion with decreased risk of suffering from a stroke. Inversely, decreased plasma antioxidant status is associated with increased neurological damage following a stroke. It was recently shown that dehydroascorbic acid, the oxidized form of vitamin C which is a superoxide scavenger, normalizes several markers of oxidative stress and inflammation in acute hyperglycemic focal cerebral ischemia in the rat (Bémeur et al., 2005). It was also demonstrated that intraventricular ascorbic acid injection is neuroprotective after hypoxic-ischemic brain injury in rats (Miura et al., 2006). Vitamin C is also able to protect the hypothalamus from oxidative stress induced in rats by an environmental toxicant (Muthuvel et al., 2006). Ascorbic acid confers protection from increased free-radical activity in the brain of spontaneously hypertensive rats by improving total antioxidant and superoxide dismutase status, thus preventing high blood pressure and its complications (Newaz et al., 2005). Also, intravenous cerebroprotective doses of citrate/sorbitol-stabilized DHA are correlated with increased brain ascorbate levels and a suppression of excessive lipid peroxidation (Mack et al., 2006). A case-control study showed that plasma vitamin C levels were lower in subjects with dementia compared to controls, which was not explained by their dietary vitamin C intakes (Charlton et al., 2004). Low brain ascorbic acid and glutathione levels associated with a perturbation of the dopaminergic system actively participate in the development of some cognitive deficits affecting schizophrenic patients (Castagné et al., 2004). It has been proposed that low ascorbate in striatal extracellular fluid may contribute to Huntington’s disease symptoms (Rebec et al., 2006) and evidence suggests that the level of extracellular ascorbate plays a critical role in regulating corticostriatal glutamate transmission (Rebec et al., 2005). A recent study suggested that ascorbate could participate in normalizing neuronal function in Huntington’s disease (Rebec et al., 2006). Antioxidant vitamins, particularly vitamins E and C may act synergistically. A short period of combined deficiency of vitamins E and C causes profound central nervous system dysfunction in guinea pigs (Burk et al., 2006). The damage consists mainly of nerve cell death, axonal degeneration, vascular injury, and associated glial cell responses. These findings suggest that the paralysis and death caused by combined deficiency of vitamins E and C in these animals is caused by severe damage to brainstem and spinal cord. Also, a recent study demonstrated that vitamin E and vitamin C prevented oxidative stress due to maternal hyperphenylalaninemia, (an inborn error of intermediary metabolism) in the brains of rat pups (Martínez- Cruz et al., 2006). Pretreatment with α-tocopherol and ascorbic acid prevents the impairment of energy metabolism caused by hyperargininemia in the cerebellum and hippocampus of rats (Delwing et al., 2006). Vitamin C and E administration, alone or in combination, increases striatal catalase activity in rats subjected to oral dyskinesias, which are implicated in a series of neuropathologies and associated with increased oxidative stress. A beneficial effect of these vitamins on reserpine- induced oral dyskinesia in rats has also been reported (Faria et al., 2005) and a recent study suggested that vitamins C and E hold promise in helping prevent AD (Frank 120 C. Bémeur et al. and Gupta, 2005). Finally, low brain glutathione and ascorbic acid l evels associated with a perturbation of the dopaminergic system may actively participate in the development of some cognitive deficits affecting schizophrenic patients (Castagné et al., 2004). 7.3 Carotenoids Carotenoids are plant pigments which constitute more than 600 compounds, most of them being lipid-soluble and which contribute significantly to the nutritional bene- fits of fruit and vegetable consumption. β-carotene is the most common form of the vitamin and is the precursor of vitamin A. β-cryptoxanthine is another precursor of vitamin A. The latter is a powerful lipid-soluble antioxidant which protects cellular membranes from oxidative stress. Vitamin A is carried into the plasma by retinal binding protein which is synthesized in the liver. Decreased carotenoid concentrations are associated with increased risk of stroke (Leppälä et al., 1999) and vitamin A levels are decreased in stroke patients (Cherubini et al., 2000). 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A short period of combined deficiency

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