HBO aftereffect on lipid peroxidation and enzyme antioxidants of the brain: prospective experiental study

OBJECTIVE. Study the effect of a single and multiple administration of hyperbaric oxygenation (HBO) in the therapeutic regime on the processes of lipid peroxidation (LPO) and enzyme of antioxidative defense in phylogenetically various structures of the brain in the period of the immediate and remote aftereffect of expositions.

MATERIALS AND METHODS. Experiments were carried out on 87 nonlinear white male rats weighing 180-230 grams. Hyperbaric oxygenation was conducted by medical oxygen in the experimental pressure chamber in the “mild” mode (2 ata, 50 min isopression), 1 session per day in the morning. The study was carried out after 1, 5, 10 sessions, in 5 and 10 days after 1 session and in 5 days after 5 sessions of HBO. The content of malondialdehyde (MDA) was determined in the brain stem, cerebellum and large brain hemispheres. The state of an enzyme element of antioxidant defense was evaluated by superoxide dismutase (SOD) and catalase.

RESULTS. It was found that exposure to oxygen under high pressure caused increased intensity of LPO processes in the brain that progresses from 1 to 5 sessions. While MDA changes in the brain stem were detected later than in the hemispheres and cerebellum. LPO intensification in the brain proceeded against the background of increased activity of SOD. After 10 sessions of HBO LPO intensity decreased that was confirmed by reduced MDA content and SOD activity in examined brain tissue. Catalase activity reduced in the stem after 5 sessions and increased in the cerebellum and hemispheres after 10 sessions of HBO. Aftereffect of 1 HBO session was characterized by persistent increase in MDA concentration in the brain regions, detected in 5 and 10 days after exposure and was accompanied by increased SOD activity against the background of reduced catalase activity. In 5 days after 5 sessions the increase in MDA content and SOD activation was observed only in the tissue of the cerebral hemispheres.

DISCUSSION. The use of HBO in the mode 2 ata, 50 min stimulates reactions of free radical oxidation (FRO) in the brain. The dynamics of their development with continued exposure shows that there are enough resources of the brain antioxidant defense to compensate hyperoxic load, including 10-fold exposure and no depletion of the reserves of enzyme antioxidant element in the brain is observed. After a single exposure of hyperbaric oxygen FRO activation remains during 10 days that can be concluded from an increased level of MDA and an increased activity of SOD in all the brain regions against the background of reduced catalase activity of stem structures and cerebellum. Repeated 5-fold exposures have a shorter metabolic “footprint”: in 5 days LPO effect and SOD activation are less pronounced than in the period of 1 session aftereffect both in 5 and 10 days.

CONCLUSION. The therapeutic “mild” mode of HBO (2 ata, 50 min, 1 session per day) causes FRO activation in the brain tissue of experimental animals. Its intensity is controlled by the activation of enzyme protection mechanisms that is enough to compensate FRO changes with this mode of hyperoxic load. After ending exposures more pronounced aftereffect of HBO in the brain regions is found after 1 session compared to 5 sessions.

marine medicine, hyperbaric oxygenation, brain, aftereffect, superoxide dismutase, antioxidants, lipid peroxidation

1. Bennett Michael. The evidence basis of diving and hyperbaric medicine: A synthesis of the high level clinical evidence with meta-analysis. 2009. 668 s.

2. Hyperbaric Oxygen Treatment in Research and Clinical Practice - Mechanisms of Action in Focus // Hyperbaric Oxygen Treatment in Research and Clinical Practice - Mechanisms of Action in Focus / pod red. Drenjančević I. London: InTech Open, 2018. DOI 10.5772/intechopen.70322

3. Pekovic S. i dr. Hyperbaric Oxygen Therapy in Traumatic Brain Injury: Cellular and Molecular Mechanisms // Hyperbaric Oxygen Treatment in Research and Clinical Practice - Mechanisms of Action in Focus. InTech, 2018.

4. Halimov YU.SH., Tkachuk N.A., ZHekalov A.N. Organizaciya i okazanie terapevticheskoj pomoshchi v sovremennyh lokal'nyh vojnah i vooruzhennyh konfliktah // Voenno-medicinskij zhurnal. 2014. T. 8. S. 16–24.

5. Susta D., Dudnik E., Glazachev O.S. A programme based on repeated hypoxia–hyperoxia exposure and light exercise enhances performance in athletes with overtraining syndrome: a pilot study // Clin. Physiol. Funct. Imaging. Blackwell Publishing Ltd, 2017. T. 37, № 3. S. 276–281. DOI: 10.1111/cpf.12296

6. Cardinale D.A., Ekblom B. Hyperoxia for performance and training // J. Sports Sci. Routledge, 2018. T. 36, № 13. S. 1515–1522. DOI: 10.1080/02640414.2017.1398893

7. Chernov V.I. i dr. Issledovanie sostoyaniya funkcij organizma vodolazov s razlichnoj ustojchivost'yu k toksicheskomu dejstviyu kisloroda // Morskaya medicina. 2022. T. 8, № 3. S. 30–39.

8. Wingelaar T.T., van Ooij P.J.A.M., van Hulst R.A. Oxygen Toxicity and Special Operations Forces Diving: Hidden and Dangerous // Front. Psychol. Front Psychol, 2017. T. 8, № JUL. DOI: 10.3389/fpsyg.2017.01263

9. Alva R. i soavt. Oxygen toxicity: cellular mechanisms in normobaric hyperoxia // Cell Biol. Toxicol. Springer Science and Business Media B.V., 2022. DOI: 10.1007/s10565-022-09773-7

10. Ay H. i soavt. Persistence of hyperbaric oxygen-induced oxidative effects after exposure in rat brain cortex tissue // Life Sci. 2007. T. 80, № 22. S. 2025–2029.

11. Fenton L.H., Robinson M.B. Repeated exposure to hyperbaric oxygen sensitizes rats to oxygen-induced seizures // Brain Res. 1993. T. 632, № 1–2. S. 143–149.

12. Simsek K. i dr. Evaluation of the Oxidative Effect of Long-Term Repetitive Hyperbaric Oxygen Exposures on Different Brain Regions of Rats // Sci. World J. 2012. T. 2012. DOI: 10.1100/2012/849183

13. Glazachev O.S. i soavt. Interval'nye gipoksicheski-giperoksicheskie trenirovki // Lechebnaya fizkul'tura i sportivnaya medicina. 2010. T. 2, № 74. S. 19–25.

14. Turovskij V.F. Vliyanie giperoksicheskoj gazovoj smesi na sostoyanie nervno-myshechnogo apparata i gemodinamiki futbolistov // Nauchnye trudy SibGUFK. 2016. S. 68–72.

15. Petrikov S.S. i soavt. Giperbaricheskaya oksigenaciya v terapii pacientov s COVID-19 // Obshchaya reanimatologiya. 2021. T. 16, № 6. S. 4–18.

16. Radchenko A.S., Shabanov P.D. Hyperoxia and hypoxia influence to adaptive processes at muscular work // Rev. Clin. Pharmacol. Drug Ther. 2018. T. 16, № 3. S. 68–77. DOI:10.17816/RCF16368-77

17. Hachaturyan M.L. i soavt. Vliyanie sezona goda na pokazateli perekisnogo okisleniya lipidov miokarda zhivotnyh s razlichnoj ustojchivost'yu k gipoksii // Byulleten' eksperimental'noj biologii i mediciny. 1995. T. 7. S. 87–90.

18. Pashkov A.I., Romanov A.Yu. Primenenie hemilyuminiscentnogo analiza dlya opredeleniya aktivnosti SOD // Byulleten' eksperimental'noj biologii i mediciny. 1990, no. 7. S. 92–94.

19. Korolyuk M.A. i soavt. Metod opredeleniya aktivnosti katalazy // Laboratornoe delo. 1988. T. 1, № 16–19.

20. Andreeva L.I. i soavt. Modifikaciya metoda opredeleniya perekisej lipidov v teste s tiobarbiturovoj kislotoj // Laboratornoe delo. 1988. T. 11. S. 41–43.

21. Jakovlev V.N., Savilov P.N., Bulgakova Y.V. Glutamate metabolism in brain structures in experimental hemorrhagic shock // Obs. Reanimatol. 2017. T. 13, № 1. DOI:10.15360/1813-9779-2017-1-6-16

22. Bulgakova YA.V., Savilov P.N. Lipid peroxidation and the antioxidant system of the rat brain during adaptation to hyperoxic load // Patologicheskaya fiziologiya i eksperimental'naya terapiya. 2022. T. 66, № 3. S. 80–90. DOI: 10.25557/0031-2991.2022.03.80-90