Melatonin info. for Marie
Posted: Tue Oct 04, 2005 8:43 am
Melatonin
Sleep disorders are common in MS, with a flattening of the normal circadian sleeping/waking rhythm, leading to wakefulness at night and somnolence during the day [Fleming WE, Pollak CP. Sleep disorders in multiple sclerosis. Semin Neurol. 2005 Mar;25(1):64-8. Review.] One cause of this may be decreased nocturnal biosynthesis of melatonin [Wu YH et al., Molecular changes underlying reduced pineal melatonin levels in Alzheimer disease: alterations in preclinical and clinical stages. J Clin Endocrinol Metab. 2003 Dec;88(12):5898-906.] Decreased melatonin biosynthesis is associated with pineal calcification [Kunz D et al., A new concept for melatonin deficit: on pineal calcification and melatonin excretion. Neuropsychopharmacology. 1999 Dec;21(6):765-72.] Pineal calcification is common in MS [Sandyk R, Awerbuch GI. The pineal gland in multiple sclerosis. Int J Neurosci. 1991 Nov;61(1-2):61-7.] Indeed, nocturnal melatonin levels were found to be lower than daytime levels in 11 of 25 patients with MS. [Sandyk R, Awerbuch GI. Nocturnal plasma melatonin and alpha-melanocyte stimulating hormone levels during exacerbation of multiple sclerosis.] Melatonin is a major antioxidant in the brain. [Reiter RJ et al., Reactive oxygen intermediates, molecular damage, and aging. Relation to melatonin. Ann N Y Acad Sci. 1998 Nov 20;854:410-24. Review.] These authors observe: 'Melatonin, the chief secretory product of the pineal gland, is a direct free radical scavenger and indirect antioxidant. In terms of its scavenging activity, melatonin has been shown to quench the hydroxyl radical, superoxide anion radical, singlet oxygen, peroxyl radical, and the peroxynitrite anion. Additionally, melatonin's antioxidant actions probably derive from its stimulatory effect on superoxide dismutase, glutathione peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase and its inhibitory action on nitric oxide synthase. Finally, melatonin acts to stabilize cell membranes, thereby making them more resistant to oxidative attack. Melatonin is devoid of prooxidant actions. In models of oxidative stress, melatonin has been shown to resist lipid peroxidation induced by paraquat, lipopolysaccharide, ischemia-reperfusion, L-cysteine, potassium cyanide, cadmium chloride, glutathione depletion, alloxan, and alcohol ingestion. Likewise, free radical damage to DNA induced by ionizing radiation, the chemical carcinogen safrole, lipopolysaccharide, and kainic acid are inhibited by melatonin. These findings illustrate that melatonin, due to its high lipid solubility and modest aqueous solubility, is able to protect macromolecules in all parts of the cell from oxidative damage. Melatonin also prevents the inhibitory action of ruthenium red at the level of the mitochondria, thereby promoting ATP production. In humans, the total antioxidative capacity of serum is related to melatonin levels. Thus, the reduction in melatonin with age may be a factor in increased oxidative damage.'
Sleep well!
Sarah
Sleep disorders are common in MS, with a flattening of the normal circadian sleeping/waking rhythm, leading to wakefulness at night and somnolence during the day [Fleming WE, Pollak CP. Sleep disorders in multiple sclerosis. Semin Neurol. 2005 Mar;25(1):64-8. Review.] One cause of this may be decreased nocturnal biosynthesis of melatonin [Wu YH et al., Molecular changes underlying reduced pineal melatonin levels in Alzheimer disease: alterations in preclinical and clinical stages. J Clin Endocrinol Metab. 2003 Dec;88(12):5898-906.] Decreased melatonin biosynthesis is associated with pineal calcification [Kunz D et al., A new concept for melatonin deficit: on pineal calcification and melatonin excretion. Neuropsychopharmacology. 1999 Dec;21(6):765-72.] Pineal calcification is common in MS [Sandyk R, Awerbuch GI. The pineal gland in multiple sclerosis. Int J Neurosci. 1991 Nov;61(1-2):61-7.] Indeed, nocturnal melatonin levels were found to be lower than daytime levels in 11 of 25 patients with MS. [Sandyk R, Awerbuch GI. Nocturnal plasma melatonin and alpha-melanocyte stimulating hormone levels during exacerbation of multiple sclerosis.] Melatonin is a major antioxidant in the brain. [Reiter RJ et al., Reactive oxygen intermediates, molecular damage, and aging. Relation to melatonin. Ann N Y Acad Sci. 1998 Nov 20;854:410-24. Review.] These authors observe: 'Melatonin, the chief secretory product of the pineal gland, is a direct free radical scavenger and indirect antioxidant. In terms of its scavenging activity, melatonin has been shown to quench the hydroxyl radical, superoxide anion radical, singlet oxygen, peroxyl radical, and the peroxynitrite anion. Additionally, melatonin's antioxidant actions probably derive from its stimulatory effect on superoxide dismutase, glutathione peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase and its inhibitory action on nitric oxide synthase. Finally, melatonin acts to stabilize cell membranes, thereby making them more resistant to oxidative attack. Melatonin is devoid of prooxidant actions. In models of oxidative stress, melatonin has been shown to resist lipid peroxidation induced by paraquat, lipopolysaccharide, ischemia-reperfusion, L-cysteine, potassium cyanide, cadmium chloride, glutathione depletion, alloxan, and alcohol ingestion. Likewise, free radical damage to DNA induced by ionizing radiation, the chemical carcinogen safrole, lipopolysaccharide, and kainic acid are inhibited by melatonin. These findings illustrate that melatonin, due to its high lipid solubility and modest aqueous solubility, is able to protect macromolecules in all parts of the cell from oxidative damage. Melatonin also prevents the inhibitory action of ruthenium red at the level of the mitochondria, thereby promoting ATP production. In humans, the total antioxidative capacity of serum is related to melatonin levels. Thus, the reduction in melatonin with age may be a factor in increased oxidative damage.'
Sleep well!
Sarah