Ascorbic acid in the brain

1993 ◽  
Vol 18 (1) ◽  
pp. 123-133 ◽  
Author(s):  
R.A. Grünewald
Keyword(s):  
Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1311
Author(s):  
Faraz Ahmad ◽  
Ping Liu

Lead (Pb) neurotoxicity is a major concern, particularly in children. Developmental exposure to Pb can alter neurodevelopmental trajectory and has permanent neuropathological consequences, including an increased vulnerability to further stressors. Ascorbic acid is among most researched antioxidant nutrients and has a special role in maintaining redox homeostasis in physiological and physio-pathological brain states. Furthermore, because of its capacity to chelate metal ions, ascorbic acid may particularly serve as a potent therapeutic agent in Pb poisoning. The present review first discusses the major consequences of Pb exposure in children and then proceeds to present evidence from human and animal studies for ascorbic acid as an efficient ameliorative supplemental nutrient in Pb poisoning, with a particular focus on developmental Pb neurotoxicity. In doing so, it is hoped that there is a revitalization for further research on understanding the brain functions of this essential, safe, and readily available vitamin in physiological states, as well to justify and establish it as an effective neuroprotective and modulatory factor in the pathologies of the nervous system, including developmental neuropathologies.


1998 ◽  
Vol 44 (1) ◽  
pp. 40-42
Author(s):  
I. P. Grigoriev

The author hypothesizes a probable causative role of alteration of ascorbic acid concentration in the brain in the development of mental disease in diabetics. In order to verify this hypothesis, ascorbic acid was measured in the brain cortex of rats 21 days after induction of streptozotocin diabetes or 1 h after intraperitoneal injection of glucose in a dose of 5 g/kg. Ascorbic acid level was increased both in diabetes (456+26 yg/g tissue versus 415+37 \vg/g in the control, p<0.01) and in acute hyperglycemia (475+54 \tg/g versus 406+65 \xg/g in the control, p<0.001). This confirmed that changed concentration of ascorbic acid in the brain can promote the development of a mental disease in diabetics. In the liver the concentration of ascorbic acid was decreased in streptozotocin diabetes (by 17%), p<0.001) and increased in acute hypoglycemia (by 24%, p<0.01). The findings permit us to hypothesize that hypoglycemia inhibits the production of ascorbic acid from the liver to the blood in rats and impedes the transport of ascorbic acid through the gut wall into the blood in humans.


2020 ◽  
Vol 715 ◽  
pp. 134656 ◽  
Author(s):  
Naoki Takeshita ◽  
Noe Kawade ◽  
Wakana Suzuki ◽  
Satoshi Hara ◽  
Fumihiko Horio ◽  
...  
Keyword(s):  

1963 ◽  
Vol 205 (6) ◽  
pp. 1073-1076 ◽  
Author(s):  
Shigeto Kanematsu ◽  
Charles H. Sawyer

A minute amount of estradiol benzoate was implanted into the posterior median eminence-basal tuberal region of the hypothalamus or hypophysis in female rabbits. Pituitary LH was measured by the ovarian ascorbic acid depletion method. Prolactin assays were performed on the same hypophyses by the intradermal pigeon crop sac method. Pituitary LH content was 0.47 µg/mg wet wt. following implantation of estrogen into parts of the brain other than the posterior median eminence-basal tuberal area. However, when estrogen was implanted into the posterior median eminence-basal tuberal area the pituitary LH content decreased markedly to less than 0.05 µg/mg and this decline was associated with ovarian atrophy. The prolactin content was significantly elevated ( P < 0.01) but the mammary glands were not activated. Estrogen implantation into the adenohypophysis appeared to cause release of prolactin but failed to affect the LH content (0.50 µg/mg) or to induce ovarian atrophy. The results indicate that estrogen acts on the posterior median eminence-basal tuberal area to stimulate production but not release of prolactin and, simultaneously, to inhibit synthesis of LH.


2015 ◽  
Vol 16 (12) ◽  
pp. 28194-28217 ◽  
Author(s):  
Adriana Covarrubias-Pinto ◽  
Aníbal Acuña ◽  
Felipe Beltrán ◽  
Leandro Torres-Díaz ◽  
Maite Castro

2015 ◽  
Vol 16 (2) ◽  
pp. 157-161 ◽  
Author(s):  
Dragan M. Pavlović ◽  
Merdin Š. Markišić ◽  
Aleksandra M. Pavlović

Abstract Vitamins are necessary factors in human development and normal brain function. Vitamin C is a hydrosoluble compound that humans cannot produce; therefore, we are completely dependent on food intake for vitamin C. Ascorbic acid is an important antioxidative agent and is present in high concentrations in neurons and is also crucial for collagen synthesis throughout the body. Ascorbic acid has a role in modulating many essential neurotransmitters, enables neurogenesis in adult brain and protects cells against infection. While SVCT1 enables the absorption of vitamin C in the intestine, SVCT2 is primarily located in the brain. Ascorbate deficiency is classically expressed as scurvy, which is lethal if not treated. However, subclinical deficiencies are probably much more frequent. Potential fields of vitamin C therapy are in neurodegenerative, cerebrovascular and affective diseases, cancer, brain trauma and others. For example, there is some data on its positive effects in Alzheimer’s disease. Various dosing regimes are used, but ascorbate is safe, even in high doses for protracted periods. Better designed studies are needed to elucidate all of the potential therapeutic roles of vitamin C.


Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1310 ◽  
Author(s):  
Jin Young Hong ◽  
Ganchimeg Davaa ◽  
Hyunjin Yoo ◽  
Kwonho Hong ◽  
Jung Keun Hyun

Axonal regeneration after spinal cord injury (SCI) is difficult to achieve, and no fundamental treatment can be applied in clinical settings. DNA methylation has been suggested to play a role in regeneration capacity and neuronal growth after SCI by controlling the expression of regeneration-associated genes (RAGs). The aim of this study was to examine changes in neuronal DNA methylation status after SCI and to determine whether modulation of DNA methylation with ascorbic acid can enhance neuronal regeneration or functional restoration after SCI. Changes in epigenetic marks (5-hydroxymethylcytosine (5hmC) and 5-methylcytosine (5mC)); the expression of Ten-eleven translocation (Tet) family genes; and the expression of genes related to inflammation, regeneration, and degeneration in the brain motor cortex were determined following SCI. The 5hmC level within the brain was increased after SCI, especially in the acute and subacute stages, and the mRNA levels of Tet gene family members (Tet1, Tet2, and Tet3) were also increased. Administration of ascorbic acid (100 mg/kg) to SCI rats enhanced 5hmC levels; increased the expression of the Tet1, Tet2, and Tet3 genes within the brain motor cortex; promoted axonal sprouting within the lesion cavity of the spinal cord; and enhanced recovery of locomotor function until 12 weeks. In conclusion, we found that epigenetic status in the brain motor cortex is changed after SCI and that epigenetic modulation using ascorbic acid may contribute to functional recovery after SCI.


Scurvy ◽  
2018 ◽  
pp. 268-276
Author(s):  
James May ◽  
Fiona Harrison

This chapter discusses the neurological basis of scurvy. The physical symptoms of extreme vitamin C deficiency, i.e., scurvy, have been described in numerous ships' logs, diaries, and medical texts, stretching back for hundreds of years. Examples include hemorrhage, and the characteristic broken blood vessels under the skin; and hyperkeratosis, or changes in hair such as thinning, alopecia, and corkscrew hairs on the limbs. However, modern techniques in neuroscience research have revealed the highly complex roles of vitamin C in the brain, which may have changed the behavior of those experiencing long periods of nutritional deficiencies. The most important roles for vitamin C, also known as ascorbate and ascorbic acid, are in the synthesis of neurotransmitters, the chemical messengers of the brain, and for protection of neurons (brain cells) against damage by a constant barrage of free radicals.


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