Ludzkie koronawirusy - autor: Krzysztof Pyrć z Zakładu Mikrobiologii, Wydział Biochemii, Biofizyki i Biotechnologii, Uniwersytet Jagielloński, Kraków

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© Borgis - New Medicine 1/2007, s. 10-14
Ewa Bartkowiak-Fludra1, *Aldona Jasińska-Stępniak1, Marek Gogolewski1, Irena Ponikowska2
Studies on the effect of ozonotherapy on blood serum α-tocopherol level in patients with atherosclerotic ischemia of lower extremities
1Department of Biochemistry and Food Analysis, Agricultural University of Poznań
2Department and Teaching Hospital of Balneology and Metabolic Diseases, University of Medicine, Bydgoszcz
Summary
Summary
The aim of the study was to investigate the destructive effect of ozone on blood serum vitamin E levels in patients with ischemia and macroangiopate dialutica of lower extremities. The primary form in blood serum is α-tocopherol [over 85%], the most biologically active tocochromanol. Sixteen assays were performed in two replications, in which blood serum concentration of vitamin E was determined at the beginning of therapy, after one infusion and after ozonotherapy was completed. Initial vitamin E concentration in the blood serum of patients showed varied vitamin E levels and the occurrence of hypovitaminosis. The action of ozone resulted in individualized vitamin E decomposition, in most cases lowering its level to one below its physiological blood serum content.
Introduction
Vitamin E active compounds, i.e. tocochromanols, are necessary for proper functioning of human and animal organisms. The biological activity of vitamin E is connected with its antioxidant properties, which protect our organisms against harmful action of forming free radicals and fatty acid peroxides [1, 5, 6].
The primary form found in blood serum (over 85%) is α-tocopherol, the most biologically active tocochromanol [moreover, the presence of α- and α-tocopherols was detected].
Alpha-tocopherol embedded into cellular membranes ensures their appropriate structure. It results in proper functioning of the hematopoietic, nervous, reproductive and cardiovascular systems, as well as muscles. It was found that vitamin E is one of the factors inhibiting the process of cell senescence [5, 12, 13].
Blood serum vitamin E concentration below 0.7 mg/dl results in shortening of erythrocyte survival time, neurological disturbances of the immune system and muscular dystrophy. Vitamin E hypovitaminosis increases the likelihood of chronic diseases of the circulatory system, skin and other metabolic disturbances [21]. A positive effect of antioxidants is shown in case of the effect of oxygen free radicals on the development of atherosclerosis. Advantages of the application of vitamin E in the prophylaxis of diseases of the cardiovascular system have been the subject of numerous studies [7]. The risk of disease due to low vitamin E levels might be of bigger importance than classical factors. It was found that low levels of α-tocopherol and ascorbate may result in early angina pectoris. In contrast, vitamin E supplementation in doses above 100 IU/d is connected with statistically significant decrease in the risk of coronary heart disease [15, 17]. Moreover, an advantageous dependency was found between vitamin E intake and the risk of death due to coronary heart disease in post-menopausal women [10].
Vitamin E deficiency may be detected on the basis of increased creatinine concentrations in urine, the erythrocyte hemolysis rate or blood serum α-tocopherol.
One of the factors having a destructive effect on vitamin E is an effect of oxidizing compounds, e.g. ozone. Ozone may oxidize physiologically important compounds and destroy organelles of living cells [3, 4, 11]. It oxidizes e.g. essential unsaturated fatty acids and tocochromanols and other important active reducing substances found in cells [1].
Appropriately selected ozone doses may have an advantageous effect on the functioning of the human organism, which has resulted in its application in the treatment of some diseases in humans and animals [14]. Ozone improves tissue oxygenation and has an advantageous effect on rheological properties of blood [16]. It may also be applied in the treatment of slowly healing wounds and bedsores, in virus and fungal infections, in obliterative thrombosis of lower extremities, in gaseous gangrene and many others, e.g. Arteriosclerosis obliterans, Macroangiopate dialutica [19].
The destructive effect of ozone on vitamin E active compounds, the appropriate blood concentrations of which determine proper functioning of the human organism, constitutes the basis for the concept for this study.
Material
Vitamin E was assayed for diagnostic purposes in patients of the Department and Teaching Hospital of Balneology and Metabolic Diseases in Ciechocinek, of the University of Medicine, Bydgoszcz, diagnosed with the ischemic disease.
A total of 28 patients with symptoms of ischemia of lower extremities due to obliterative atherosclerosis and diabetic macroangiopathy, treated at the above mentioned Department and Teaching Hospital, were included in the study.
Three groups were distinguished out of the patients:
– patients with ischemia of lower extremities – the control group (4 patients not subjected to ozonotherapy);
– patients with ischemia of lower extremities – the experimental group (16 patients undergoing ozonotherapy);
– patients with ischemia of lower extremities – the experimental group (4 patients 10-day vitamin E supplementation in the amount of 200 mg/day and treatment with oxygen-ozone mixture);
– patients with ischemia of lower extremities – the experimental group (4 patients 10-day vitamin E supplementation in the amount of 500 mg/day and treatment with oxygen-ozone mixture).
The patients were 38-75 years old (±60.54 years of age).
The clinical characteristics of the patients, apart from the type of disease, included also the body mass index (BMI), the ankle/shoulder index [A/S index] and total cholesterol (Tables 1 and 2).
Table 1.Clinical characteristics of patients.
No.AgeBMI*Diabetes treatmentA/S Index** before treatmentA/S Index after treatmentTotal cholesterolType of vascular disease
beforafterR1L2R1L2beforeafterAO1MD2
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
53
55
56
47
53
71
75
71
60
61
55
63
69
59
74
67
32.0
26.7
32.8
26.2
23.2
22.9
22.3
33.2
20.7
24.0
28.0
24.8
28.0
25.7
34.1
28.5
30.0
27.2
30.5
25.2
22.7
22.1
21.9
31.0
20.6
24.0
26.6
24.2
28.0
24.6
32.6
27.8

Tablets
Insulin
-
-
-
-
-
Tablets
-
-
-
Insulin
-
Insulin
-
Insulin

0.94
-
0.78
0.85
-
-
0.80
1.00
1.03
0.65
0.81
-
0.56
0.53
1.02
0.50
0.70
-
0.57
0.76
-
-
0.70
0.90
1.06
0.78
0.66
-
0.50
0.93
1.03
0.80
1.06
-
0.84
0.92
-
-
0.80
0.93
1.07
0.69
0.78
-
0.58
0.76
1.00
0.44
0.90
-
0.61
0.76
-
-
0.80
0.93
1.06
0.83
0.69
-
0.66
0.96
1.06
0.86
214
276
185
307
251
219
238
212
202
248
245
202
192
266
212
189
195
289
173
333
253
230
237
186
221
258
218
206
204
276
203
205


AO
AO
AO
AO

AO
AO
AO

AO
AO


MD
MD





MD



MD

MD
MD
MD
Control group
1 control
2 control
3 control
4 control
52
60
55
74
35.1
31.3
22.9
26.6
33.50
30.0
22.7
25.8
Insulin
Tablets
-
Insulin
0.68
0.94
-
0.36
0.72
0.87
0.96
0.94
0.71
0.96
-
0.37
0.75
0.97
0.93
0.48
190
196
295
211
171
209
303
208


AO
AO
MD
MD

BMI* – Body mass index [kg/m2] 25 kg – overweight
AO1 – Arteriosclerosis obliterans
MD2 – Macroangiopate dialutica
A/S.Index** – ankle/shoulder-index; R1 – right, L2 – left
Table 2. Clinical characteristics of patients with vitamin E supplementation in the diet (200 mg and 500 mg/day).
No.AgeBMI*Diabetes treatmentA/S Index** before treatmentA/S Index after treatmentTotal cholesterolType of vascular diseaseDose/daily intake
beforeafterR1L2R1L2beforeafterAO1MD2
1200
2200
3200
4200
38
65
45
62
23.0
26.3
25.3
26.6
22.5
26.4
25.0
26.2
-
Insulin
-
-
0.81
0.92
0.40
0.56
0.34
0.60
0.96
0.60
1.00
0.94
0.46
0.65
0.50
0.64
0.93
0.67
262
267
261
243
269
233
271
253
AO

AO
AO

MD

200 mg/day
5500
6500
7500
8500
63
63
60
69
37.0
31.6
27.0
15.3
36.7
30.2
27.2
15.5
Insulin
Insulin
Insulin
-
-
0.62
 
-
1.06
0.96
-
-
0.85
-
-
-
1.23
1.10
-
258
206
243
213
209
213
250
225



AO
MD
MD
MD
500 mg/day
BMI* – Body mass index [kg/m2] 25 kg – overweight
AO1 – Arteriosclerosis obliterans
MD2 – Macroangiopate dialutica
A/S.Index** – ankle/shoulder-index; R1 – right, L2 – left
Methods
The control group consisted of 4 patients (not subjected to ozonotherapy).
Ozonotherapy was administered in case of 16 patients. Assays were performed in three replications, in which blood serum α-tocopherol concentration was determined before the beginning of therapy, after 1 day of therapy and after ozonotherapy was concluded (day 10). The investigations included also 4 patients, which were administered 200 mg vitamin E throughout therapy and 4 patients with diet supplementation of 500 mg vitamin E per day.
The procedure consisted in the dissolution of the oxygen-ozone mixture in isotonic salt solution. The oxygen-ozone mixture contained 95% oxygen and 5% ozone, with ozone concentration of 40-45 μl per 1 cm3 gas. After 10 min ozonization, ozone was dissolved in isotonic salt solution (500 cm3) in the amount of 2000 to 2200 pg. On average the drip infusion lasted for 40-60 minutes. While it was being administered some of the ozone from the solution decomposed and volatilized. In order to maintain the original ozone concentration throughout the administration of the drip infusion the solution was ozonized with the oxygen-ozone mixture.

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Piśmiennictwo
1. Bartosz G. Druga twarz tlenu. PWN, Warszawa, 1995; 13-295. 2. Bartkowiak-Fludra E. Wpływ wybranych czynników fizyko-chemicznych na tokoferole. Praca doktorska. AR Poznań, 2004. 3. Bocci V. Oxygen - Ozone Therapy: A Critical evaluation. Kluwer Academic Publishers, Medical/Nursing, 2002. 4. Bocci V. Ozone as a bioregulator. Pharmacology and toxicology of ozonetherapy today. J. Biol. Regul Homeost Agents, 1996, 10 [2-3]: 31-53. 5. Combs G.F. Vitamin E, in The Vitamins: Fundamental Aspects in Nutrition and Health. Academic Press Inc., San Diego, 1992. 6. Denisov E.T., Khudykov I.V. Mechanisms of action and reactivities of free radicals of inhibitors. Chem. Revs.,1987; 87: 1313-1357. 7. Gey K., Pusaka P. Vitamin E and vitamin C supplementation. Ann. NY Acad. Sci., 1990; 57: 268-282. 8. Gomez M.F.D., Sazatornil J.A.G., Rosales F.H., Rubi W.D. Effect of a-tocopherol during in vitro ozonation of methyl linoleate: its implication in ozone. Ozone: Science and engineering, 2004; 26: 189-194. 9. Hernandez F., Menendez S., Wong R. Decrease of blood cholesterol and stimulation of antioxidative response in cardiopathy patients treated with endogenous ozone therapy. Free Radical biology and Medicine, 1995; 19, 1: 115-119. 10. Kushi L.H., Folsom A.R., Prineas R.J. Dietery antioxidant vitamins and death from coronary heart disease in posmenopausal women. N. Engl J. Med., 1996; 334: 1152-1163. 11. Liebler D., Matsumoto S., Iitaka Y., Matsuo M. Reaction of vitamin E and ist model compound 2,2,5,7,8-Pentamethylchroman-6-ol with ozone. Chemical Research in Toxicology, 1993; 6: 69-72. 12. Nogala-Kalucka M., Gogolewski M. Związki witamino-E aktywne i ich znaczenie. Polskie Towarzystwo Technologów Żywności, Poznań, 1994; 4. 13. Packer L. Protective Role of Vitamin E in Biological Systems. Am. J. Clin. Nutr., 1991; 53: 1050-1055. 14. Rilling S., Viebahn R. Praxis der Ozon-Sauerstoff-Therapie. Heidelberg, 1990; 48-55. 15. Rimm E.B., Stampfer M.J., Ascherio A. Vitamin E consumption and the risk of coronary disease in men. N Engl. J. Med. , 1993; 328: 1450-1456. 16. Rokitansky O. Der biochemische wirkungs-mechanism der Ozon-Sauerstoff gemisches in blut. Der directe erythrozytare mechanismus. Kongresbericht zur Ozontherapie. Baden-Baden, 1981. 17. Stampfer M.J., Hennekens C.H., Manson J.E. Vitamin E consumption and the risk of coronary disease in women. N Engl. J. Med. , 1993; 328: 1444-1449. 18. Thiele J.J., Traber M.G., Polefka Th.G., Cross C.E., Packer L. Ozone-Exposure Depletes Vitamin E and Induces Lipid Peroxidation in Murine Stratum Corneum. J. Invest Dermatol., 1997; 107: 753-757. 19. Turczyński B. Bezpośredni i odległy wpływ ozonoterapii na lepkość krwi i dystans chromania przystankowego u chorych na cukrzycę. Ann. Acad. Med. Siles., 1992; 25, 105. 20. Włodarczyk K. Badanie enzymów układu antyoksydacyjnego u chorych z przewlekłym niedokrwieniem kończyn dolnych poddanych terapii ozonowej. Praca doktorska. AM Bydgoszcz, 2001. 21. Ziemlański S., Budzyńska-Topolowska J. Tłuszcze pożywienia i lipidy ustrojowe. PWN Warszawa, 1991; 376-388.
Adres do korespondencji:
*Aldona Jasińska-Stępniak
60-623 Poznan, Poland, Mazowiecka Str. 48
tel.+48/61/8487350, fax +48/61/8487352
e-mail: aldonajs@au.poznan.pl

New Medicine 1/2007
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