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 »  Results
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Year : 2003  |  Volume : 51  |  Issue : 2  |  Page : 220-222

Plasma antioxidant vitamins in brain tumors

Department of Biochemistry, Kasturba Medical College and Hospital, Manipal-576104

Correspondence Address:
Department of Biochemistry, Kasturba Medical College, Mangalore
dr[email protected]

  »  Abstract

Plasma levels of vitamins A, E and C were analyzed in 102 patients with different types of brain tumors. A follow-up study was done with 27 postoperative patients. On comparison with plasma from normal individuals, vitamin A and E were decreased, but the decrease was statistically insignificant. Vitamin C levels remained in the normal range. In a comparative study of preoperative and postoperative cases, plasma vitamin A levels in postoperative glioma patients were significantly higher than those in the pre-operative state. There was no significant difference in the plasma level of vitamins C and E. The results of the present study suggest that the plasma antioxidant vitamins are not altered effectively in brain tumor cases.

How to cite this article:
Rao G, Rao A, Raja A, Rao S, Rao A. Plasma antioxidant vitamins in brain tumors . Neurol India 2003;51:220-2

How to cite this URL:
Rao G, Rao A, Raja A, Rao S, Rao A. Plasma antioxidant vitamins in brain tumors . Neurol India [serial online] 2003 [cited 2023 Feb 6];51:220-2. Available from: https://www.neurologyindia.com/text.asp?2003/51/2/220/1089

There is growing evidence implicating free radicals in a wide variety of medical diseases and conditions such as cancer and cardiovascular diseases. Epidemiological findings and animal studies support the belief that vitamins protect against cardiovascular diseases and probably cancer.[1] Vitamin A and carotenoids have been considered antioxidants because of their capacity to relieve oxidative stress.[2],[3] They prevent lipid peroxidation by scavenging free radicals and other reactive oxygen species.[4] Moreover, the vitamin has been implicated as a biological factor in reducing the incidence of cancer.[5] Vitamin E is a lipid soluble chain breaking antioxidant.[6] It may have an implication in the prevention of Alzheimer's disease, coronary heart disease and pretreatment may be a valuable method for myocardial protection.[7],[8] Pre-treatment of animals with a-tocopherol has been reported to lessen secondary damage in several models of ischemic or traumatic injury to CNS.[9],[10] An increase in vitamin E is observed in esophageal cancer.[11] Several studies found lower plasma vitamin E in patients with existing lung cancer and oral cancer.[12],[13],[14] Ascorbate reacts rapidly with superoxide and peroxyl radicals and even more rapidly with hydroxyl radicals to give semidehydroascorbate. Ascorbate can diminish the carcinogenicity of nitrosocompounds by reducing the nitroso group to an inactive product or by diminution of endogenous fecal mutagens.[15],[16] It has been established that a significantly increased relative risk of gastrointestinal cancer exists at low concentration of vitamin C.[17],[18],[19] Furthermore, deficiency of vitamin C causes oxidative DNA damage and impaired immune response.[15],[16],[20]
There are no reports on plasma levels of vitamins A and E, and very few on levels of vitamin C in patients with brain tumor. In the present study, an attempt has been made to assess the plasma antioxidant vitamin status in such patients and evaluate the possibility of their role in preventing oxidative damage.

   »   Material and Methods

Plasma samples from 102 patients, aged between 40-80 years, with different types of brain tumors including glioma, meningioma, acoustic neurinoma and other types (secondary tumors, tuberculoma, lymphoma, ventricular tumor and craniopharyngioma, [Table - 1]), were studied. Healthy subjects (n=47) matched for age and sex were also studied as a control group during this period. Postoperative blood samples were obtained from the patients when they were reexamined at a follow-up study. Blood was collected in EDTA bottles. It was immediately centrifuged under refrigeration at 3000g for 10 minutes. The plasma was carefully separated and the vitamins estimated immediately.
The estimation of vitamin A was done by the method of Paterson and Wiggins.[21] Vitamin E levels were determined by the method of Bieri et al.[22] Vitamin C was estimated chemically by using dinitrophenylhy-drazine as a color compound.[23] Statistical analysis was done according to Student's paired and unpaired 't' test.

   »   Results  Top

The plasma vitamin A and vitamin E levels showed a tendency to decrease in most of the brain tumor patients except in acoustic neurinoma, where the mean values showed a tendency to increase. However, a statistically significant difference was not observed in any of the study groups, when compared with the control group. Vitamin C levels remained in the normal range [Table - 2]. A drop in the mean plasma vitamin A and tocopherol levels was observed in both, benign and malignant brain tumor patients when compared to controls but this was not statistically significant. Low levels of plasma ascorbate were observed in patients with benign lesions whereas those with malignant tumors showed an increase in the vitamin C levels when compared to the controls. The increase in plasma ascorbate levels in patients with malignant tumors was significant (p < 0.005) when compared to those with benign lesions [Table - 3]. In the follow-up study, plasma vitamin A levels in postoperative glioma patients were significantly higher (p < 0.02) than those in the preoperative state. There was no statistically significant difference in plasma vitamin E and vitamin C levels in a comparative study of preoperative and postoperative samples [Table - 4].

   »   Discussion Top

Retinol has long been known to be an effective antioxidant because of its capacity to scavenge free radicals. By quenching free radicals it protects lipids against peroxidation. Comstoc et al[24] observed low levels of retinol and b-carotene in patients with cancer. Stone and Troll[25] reported that retinol and its analogues, retinyl acetate and retinoic acids are effective inhibitors of superoxide radical production in polymorphonuclear leukocytes. A high serum vitamin A concentration has been reported to have a beneficial effect on the outcome of ischemic stroke.[26] It has been established that there is a significantly increased relative risk of gastrointestinal cancer at low levels of vitamin A.[27] This report is similar to the findings in the present study of low levels of plasma vitamin A in most brain tumors. Vitamin A deficiency is well known to result in metaplasia and facilitation of tumors in experimental animals. In humans, vitamin A and b-carotene reverse precancerous leukoplakia and reduce the occurrence of pathological micronuclei even on continuous exposure to mutagens from betel-nuts and tobacco chewing.[28] Faber et al,[29] in their preliminary study, reported that the plasma vitamin A level was not modified either in patients with cancer or after chemotherapy.
Numerous studies have evaluated the neuroprotective efficiency of pharmacological agents with lipid antioxidant activity in models of spinal cord and brain injury. A decrease in lipid peroxidation and an increase in the activity of antioxidant enzymes have been observed after the administration of a-tocopherol and Se during the treatment of brain impairment.[9] Intensive pretreatment of animals with endogenous lipid peroxyl radical scavenger, a-tocopherol, with 21-aminosteroids has been shown to decrease post-traumatic spinal ischemia and enhance chronic neurological recovery.[9],[10] Low levels of plasma vitamin E levels, as shown in our study, may facilitate oxidative damage in these patients.
A protective effect on lipid peroxidation of vitamin C has been well established by Simon[30] and Matsuda et al.[31] Vitamin C may help to reduce the free radical damage and atheroma formation in blood vessels.[32] Significantly reduced vitamin C levels have been reported in astrocytomas.[33] The plasma vitamin C levels in cases of brain tumor in this study were within normal limits. Moreover, the marked increase in vitamin C levels in malignant cases over those observed in benign tumors may be due to the fact that more of ascorbic acid is used to regenerate vitamin E in membranes in these cases.[34]
The patients and controls in this study belonged to a homogeneous population with no differences in their cultural or socio-economic status. Hence, nutritional differences between the two groups are minimal. Therefore, the results of the present study suggest that the plasma antioxidant vitamins are not affected much in brain tumors. However, this does not overrule any possibility of alteration of vitamins at the site of the tumor. Further, the decreased activity of antioxidant enzymes[35] accompanied with increased lipid peroxidation[36] may be the major factors responsible for the oxidative stress observed in these cases. 

  »   References Top

1.Packer L. Protective role of vitamin E in biological systems. Am J Clin Nutr 1991;53:1050s-55s.  Back to cited text no. 1    
2.Krinsky NI. Carotenoid protection against oxidation. Pure Appl Chem 1979;51:649-60.  Back to cited text no. 2    
3.Krinsky NI, Deneke SM. Interaction of oxygen and oxyradicals with carotenoid. J Natl Cancer Inst 1982;69:205-9.  Back to cited text no. 3    
4.Kartha VNR, Krishnamurthy S. Antioxidant function of vitamin A. Int J Vitam Nutr Res 1977;47:394-401.   Back to cited text no. 4    
5.Peto R, Doll R, Buckley JD, et al. Can dietary beta-carotene materially reduce human cancer rates? Nature 1981;290:201-8.   Back to cited text no. 5  [PUBMED]  
6.Burton GW, Vitamin E. Molecular and biological function. Proc Nutr Soc 1994;53:251-62.  Back to cited text no. 6    
7.Behn C, Davis J, Cole GM, et al. Vitamin E protects nerve cells from amylioid beta protein toxicity. Biochem Biophys Res Commun 1992;186:944-50.  Back to cited text no. 7    
8.Henriksen T, Endersen M. Oxidative stress and antioxidants. Tidsskr Nor Lageforen 1994;114:328-30.  Back to cited text no. 8    
9.Dzhandzhgava TG, Shakarishivilli RR. Activity of antioxidant protective enzymes and content of lipid peroxidation products in blood serum and cerebrospinal fluid in patients with ischemic heart disease. Vopr Med Khim 1992;38:33-5.  Back to cited text no. 9    
10.Hall ED, Yonkers PA, Andrus PK, et al. Biochemistry and pharmacology of lipid peroxidants in acute brain and spinal cord injury. J Neurotrauma 1992;9:425s-42s.  Back to cited text no. 10    
11.Kavamura T, Ohisha Y, Abe Y, et al. Plasma lipid peroxides in the operation of esophageal cancer. Rinsho Byori 1992;40:881-4.  Back to cited text no. 11    
12.Miyamoto H, Aroya Y, I to M. Serum selenium and vitamin E concentrations in families of lung cancer patients. Cancer 1987;60:1159-62.  Back to cited text no. 12    
13.Legardeur BY, Lopez SA, Johnson WD. A case control study of serum vitamin A, E and C in lung cancer patients. Nutr Cancer 1990;14:130-40.  Back to cited text no. 13    
14.Harris RWC, Key TJA, Silooks PB, et al. A case control study of dietary carotene in men with lung cancer and in men with oral epithelial cancer. Nutr Cancer 1991;15:63-8.  Back to cited text no. 14    
15.Machlin LJ. In: Decker NY, editor. Handbook of vitamins. New York: Academic Press; 1991.  Back to cited text no. 15    
16.Gaby S, Bendich A, Singh VN, et al. Vitamin intake and death. A scientific review. In: Decker NY, editor. Handbook of vitamins. New York: Academic Press; 1991; pp. 145-70.   Back to cited text no. 16    
17.Stahelin HB, Gey KF, Brucher GB. Plasma vitamin C and cancer death. The prospective basal study. Ann N Y Acad Sci 1987;498:124-31.  Back to cited text no. 17    
18.Gey KF, Braucher GB, Stehelin HB, et al. Plasma levels of antioxidant vitamins in relation to ischemic heart disease and cancer. Am J Clin Nutr 1987;5:1368-77.  Back to cited text no. 18    
19.Gey KF, Stahelin HB, Braucher GB. Plasma levels of essential antioxidants inversely related to subsequent cancer. In: Hayashi O, Niki E, Kondo M, editors. Medical, biochemical and chemical aspects of free radicals. Amsterdam: Elsevier Science Publishing Company; 1989. pp. 377-84.  Back to cited text no. 19    
20.Jacob RA, Keley DS, Painetto FS. Immunocompetence and oxidant defence during ascorbate depletion of healthy men. Am J Clin Nutr 1991;53:194-200.  Back to cited text no. 20    
21.Paterson JCS, Wiggins HS. An estimation of plasma vitamin A and the vitamin. A absorption test. J Clin Pathol 1954;7:56-60.  Back to cited text no. 21    
22.Bieri JG, Teetz L, Belvady B, et al. Serum vitamin E levels in normal adult population in Washington DC. Arch Proc Soc Exp Biol Med 1964;117:131-3.  Back to cited text no. 22    
23.Omaye ST, Turnbull JD, Sauberlich HE. Selected methods for the determination of ascorbic acid in animal cells, tissues and fluids. Methods Enzymol 1979; 62:3-11.  Back to cited text no. 23    
24.Comstoc GW, Helzlsour KJ, Bush TL. Pre-diagnostic serum levels of carotenoids and vitamin E as related to subsequent cancer in Washington country. Maryland. Am J Clin Nutr 1991;53:2605-15.  Back to cited text no. 24    
25.Stone DS, Troll M. Retinoid inhibition of superoxide anion radical production by human polymorphonuclear leukocyte stimulated with tumour promoter. Biochem Biophys Res Commun 1980;97:883-8.  Back to cited text no. 25    
26.Dekeyser J, Deklippel N, Merk H, et al. Serum concentrations of vitamin A and vitamin E and early outcome after ischemic stroke. Lancet 1992;339:1562-5.  Back to cited text no. 26    
27.Sthelin HB, Gey KF, Eichholzer M. Plasma antioxidant vitamins and subsequent cancer motility in 12 year follow up of the prospective study. Am J Epidemol 1991;133:766-75.  Back to cited text no. 27    
28.Stitch H, Matthew B, Sankaranarayana R, et al. Remision of pre-cancerous lesions in the oral cavity of tobacco chewers and maintenance of protective effects of E1-carotene and vitamin A. Am J Clin Nutr 1991;53:238-46.  Back to cited text no. 28    
29.Faber M, Coudary C, Hida M, et al. Lipid peroxidation products and vitamin and trace element status in patients with cancer before and after chemotherapy including adriamycin, a preliminary study. Biol Trace Elem Res 1995;117-23.  Back to cited text no. 29    
30.Simon JA. Vitamin C and cardiovascular disease: A review. J Am Coll Nutr 1992;11:107-25.  Back to cited text no. 30    
31.Matsuda T, Tanaka H, Yuasa H, et al. The effect of high dose vitamin C on post-burn lipid peroxidation. Burn Care Rehabil 1993;14:624-9.  Back to cited text no. 31    
32.MacMury SM, Muir M, Hume R. Seasonal and climate variation in cholesterol and vitamin C: effect of vitamin C supplementation. Scott Med J 1992;37:49-52.  Back to cited text no. 32    
33.Landolt H, Langermann H, Probst A, et al. Levels of water soluble antioxidant in asrocytoma and adjacent tumour free tissue. J Neurooncol 1994;21:127-33.  Back to cited text no. 33    
34.Halliwell B, Gutteridge JMC. Oxygen is poisonous-An introduction to oxygen toxicity and free radicals. In: Halliwell B, Gutteridge JMC, editors. Free radicals in biology and medicine. 2nd edn. Oxford: Clarendon Press; 1991; pp. 1-20.   Back to cited text no. 34    
35.Rao GM, Rao AV, Raja A, et al. Role of antioxidant enzymes in brain tumours. Clin Chim Acta 2000;296:203-12.  Back to cited text no. 35    
36.Rao GM, Rao AV, Raja A, et al. Lipid peroxidation in brain tumours. Clin Chim Acta 2000;302:205-11.  Back to cited text no. 36    


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