J Clin Neurol.  2016 Oct;12(4):414-418. 10.3988/jcn.2016.12.4.414.

Effects of Regular Treadmill Exercise on a DNA Oxidative-Damage Marker and Total Antioxidant Capacity in Rat Hippocampal Tissue

• Mahjoub S
• Ghadi A
• Pourbagher R
• Hajian-Tilaki K
• Masrour-Roudsari J

• KMID: 2385104
• DOI: http://doi.org/10.3988/jcn.2016.12.4.414

Abstract

BACKGROUND AND PURPOSE
Regular exercise can result in changes in the levels of oxidative stress in the hippocampus; however, little attention has been paid to physical-activity-induced neuronal protection to exposure to lead compounds. This study investigated the effects of regular treadmill exercise on a DNA oxidative-damage marker [8-hydroxy-2'-deoxyguanosine (8-OHdG)] and the total antioxidant capacity (TAC) of hippocampal tissue in lead-acetate exposed rats.
METHODS
This study investigated the effects of 8 weeks of regular treadmill exercise on 8-OHdG and the TAC of hippocampal tissue in lead-acetate-exposed rats. Wistar rats were randomly divided into four groups: baseline, sham (control), lead, and exercise+lead. The exercise program involved running on a treadmill with increasing intensity five times a week for 8 weeks. Animals in the lead and exercise+lead groups received lead acetate at 20 mg/kg body weight intraperitoneally three times weekly for 8 weeks. Animals in the sham group received solvent (ethyl oleate) at 30 mg/kg body weight three times weekly for 8 weeks. TAC and 8-OHdG were measured by spectrophotometric and ELISA techniques, respectively. Data were analyzed by ANOVA and Tukey's post-hoc test with a significance cutoff of p≤0.05.
RESULTS
The level of 8-OHdG and the TAC were significantly higher and lower, respectively, in the lead group than in the baseline and sham groups (p<0.01). However, the 8-OHdG level and TAC value in hippocampal tissue were significantly decreased and increased, respectively, in the exercise+lead group relative to the lead group (p<0.05).
CONCLUSIONS
The TAC of hippocampal tissue may be directly associated with neural protection mechanisms of exercise following lead acetate injection, and the beneficial effects of regular exercise in preventing hippocampal neuronal damage could be due to decreased hippocampal oxidative stress such as reflected by a lower 8-OHdG level and increased TAC.

Keyword

regular treadmill exercise; total antioxidant capacity; 8-OHdG; hippocampus; lead acetate; oxidative stress

MeSH Terms

Animals
Body Weight
DNA*
Enzyme-Linked Immunosorbent Assay
Hippocampus
Neurons
Neuroprotection
Oxidative Stress
Rats*
Rats, Wistar
Running
DNA

Reference

1. Roceri M, Hendriks W, Racagni G, Ellenbroek BA, Riva MA. Early maternal deprivation reduces the expression of BDNF and NMDA receptor subunits in rat hippocampus. Mol Psychiatry. 2002; 7:609–616.

2. White LD, Cory-Slechta DA, Gilbert ME, Tiffany-Castiglioni E, Zawia NH, Virgolini M, et al. New and evolving concepts in the neurotoxicology of lead. Toxicol Appl Pharmacol. 2007; 225:1–27.

3. Dabidi RV, Hosseinzadeh S, Mahjoub S, Hosseinzadeh M, Myers J. Endurance exercise training and diferuloyl methane supplement: changes in neurotrophic factor and oxidative stress induced by lead in rat brain. Biol Sport. 2013; 30:41–46.

4. Hosseinzadeh S, Roshan VD, Mahjoub S. Continuous exercise training and curcumin attenuate changes in brain-derived neurotrophic factor and oxidative stress induced by lead acetate in the hippocampus of male rats. Pharm Biol. 2013; 51:240–245.

5. Cechetti F, Rhod A, Simão F, Santin K, Salbego C, Netto CA, et al. Effect of treadmill exercise on cell damage in rat hippocampal slices submitted to oxygen and glucose deprivation. Brain Res. 2007; 1157:121–125.

6. Leeuwenburgh C, Heinecke JW. Oxidative stress and antioxidants in exercise. Curr Med Chem. 2001; 8:829–838.

7. Ficicilar H, Zergeroglu AM, Tekin D, Ersoz G. The effects of acute exercise on plasma antioxidant status and platelet response. Thromb Res. 2003; 111:267–271.

8. Ficicilar H, Zergeroglu AM, Ersoz G, Erdogan A, Ozdemir S, Tekin D. The effects of short-term training on platelet functions and total antioxidant capacity in rats. Physiol Res. 2006; 55:151–156.

9. Trombini TV, Pedroso CG, Ponce D, Almeida AA, Godinho AF. Developmental lead exposure in rats: is a behavioral sequel extended at F2 generation? Pharmacol Biochem Behav. 2001; 68:743–751.

10. Toyokuni S, Tanaka T, Hattori Y, Nishiyama Y, Yoshida A, Uchida K, et al. Quantitative immunohistochemical determination of 8-hydroxy-2'-deoxyguanosine by a monoclonal antibody N45.1: its application to ferric nitrilotriacetate-induced renal carcinogenesis model. Lab Invest. 1997; 76:365–374.

11. Benzie IF, Strain JJ. The ferric reducing ability of plasma (FRAP) as a measure of "antioxidant power": the FRAP assay. Anal Biochem. 1996; 239:70–76.

12. Dietert RR, Lee JE, Hussain I, Piepenbrink M. Developmental immunotoxicology of lead. Toxicol Appl Pharmacol. 2004; 198:86–94.

13. Ahamed M, Siddiqui MK. Environmental lead toxicity and nutritional factors. Clin Nutr. 2007; 26:400–408.

14. Aykin-Burns N, Laegeler A, Kellogg G, Ercal N. Oxidative effects of lead in young and adult Fisher 344 rats. Arch Environ Contam Toxicol. 2003; 44:417–420.

15. Ling Z, Gayle DA, Ma SY, Lipton JW, Tong CW, Hong JS, et al. In utero bacterial endotoxin exposure causes loss of tyrosine hydroxylase neurons in the postnatal rat midbrain. Mov Disord. 2002; 17:116–124.

16. Karpuzoglu-Sahin E, Hissong BD, Ansar Ahmed S. Interferon-gamma levels are upregulated by 17-beta-estradiol and diethylstilbestrol. J Reprod Immunol. 2001; 52:113–127.

17. Jaako-Movits K, Zharkovsky T, Romantchik O, Jurgenson M, Merisalu E, Heidmets LT, et al. Developmental lead exposure impairs contextual fear conditioning and reduces adult hippocampal neurogenesis in the rat brain. Int J Dev Neurosci. 2005; 23:627–635.

18. Duman RS, Malberg J, Nakagawa S. Regulation of adult neurogenesis by psychotropic drugs and stress. J Pharmacol Exp Ther. 2001; 299:401–407.

19. Aguiar AS Jr, Tuon T, Pinho CA, Silva LA, Andreazza AC, Kapczinski F, et al. Intense exercise induces mitochondrial dysfunction in mice brain. Neurochem Res. 2008; 33:51–58.

20. Radák Z, Kaneko T, Tahara S, Nakamoto H, Pucsok J, Sasvári M, et al. Regular exercise improves cognitive function and decreases oxidative damage in rat brain. Neurochem Int. 2001; 38:17–23.

21. Shahandeh M, Dabidi Roshan V, Mahjoub S, Sarkisian V. Can aerobic training restore the level of BDNF in the hippocampus of rats exposed to lead acetate? New Armen Med J. 2011; 5:4–11.

22. Shahandeh M, Roshan VD, Hosseinzadeh S, Mahjoub S, Sarkisian V. Chronic exercise training versus acute endurance exercise in reducing neurotoxicity in rats exposed to lead acetate. Neural Regen Res. 2013; 8:714–722.