Effects of exhaustive exercise and vitamin B6 deficiency on free radical oxidative process in male trained rats.
There is growing evidence that oxygen free radical production and subsequent lipid peroxidation are normal sequelae to the rise in oxygen consumption concomitant with exercise. In addition, increased lipid peroxidation has also been shown in vitamin B6-deficient rat plasma, liver, and kidney. To investigate the potential for a role of vitamin B6 in exercise-induced oxidative stress, 36 male Sprague-Dawley rats received 0 (n = 12), 2 (n = 12), and 8 mg pyridoxine (PN)-HCl/kg diet (n = 12) and were trained by a 9-week swimming program. After 9-weeks of training, six rats (exhausted: E rats) of each vitamin group were exercised to exhaustion by swimming while the other six rats rested (nonexhausted: NE rats). Ascorbate, ascorbate free radical and antilipoperoxidant capability (AC) were evaluated in plasma. These parameters were higher in E rats than in NE rats. Free radical-mediated lipid peroxidation was measured in tissue and plasma by evaluation of thiobarbituric acid reactive substances (TBARS) content. This index of peroxidation was significantly increased in liver of E rats but not in plasma, heart, and gastrocnemius muscle. Concentration of TBARS in liver was the highest in vitamin B6-deficient rats (consuming 0 mg PN-HCl/kg diet) and the lowest in vitamin B6-sufficient rats (consuming 8 mg PN-HCl/kg diet). Vitamin E (alpha-tocopherol) levels in liver and heart were negatively related to vitamin B6 levels in the diet. Independently of vitamin B6, liver and muscle alpha-tocopherol levels were significantly higher in E animals than in NE animals. There is good evidence according to our results that exercise induced an oxidative stress, as indicated by a significant increase of ascorbyl radical levels in the plasma. The effects of vitamin B6 deficiency on the free radical metabolism are low in trained rats. On the contrary, exhaustive exercise induced modifications in the metabolism pathways of vitamin C and E objectivated by variations of levels of vitamin C in the plasma and vitamin E in liver.
Benderitter
M
M
Laboratoire de Physiopathologie et Pharmacologie Cardiovasculaires Expérimentales, Facultés de Médecine et de Pharmacie, Dijon, France.
Hadj-Saad
F
F
Lhuissier
M
M
Maupoil
V
V
Guilland
J C
JC
Rochette
L
L
D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000097:blood*; D001835:Body Weight / Q000187:drug effects; D003683:Dehydroascorbic Acid / Q000031:analogs & derivatives / Q000097:blood; D005609:Free Radicals / Q000378:metabolism; D006321:Heart / Q000033:anatomy & histology / Q000187:drug effects; D007501:Iron / Q000097:blood; D015227:Lipid Peroxidation; D008099:Liver / Q000033:anatomy & histology / Q000187:drug effects; D008297:Male; D018482:Muscle, Skeletal / Q000033:anatomy & histology / Q000187:drug effects; D009929:Organ Size / Q000187:drug effects; D010101:Oxygen Consumption; D010805:Physical Conditioning, Animal; D005082:Physical Exertion; D011736:Pyridoxine / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013550:Swimming; D013997:Time Factors; D026681:Vitamin B 6 Deficiency / Q000503:physiopathology*; D014810:Vitamin E / Q000097:blood
D000975:Antioxidants; D005609:Free Radicals; D014810:Vitamin E; C000820:semidehydroascorbic acid; D007501:Iron; D011736:Pyridoxine; D001205:Ascorbic Acid; D003683:Dehydroascorbic Acid