Abstract
1/2013
vol. 30
Original paper
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
Online publish date: 2014/07/22
Lead is a highly neurotoxic agent that particularly affects the developing central nervous system.
In the current study we investigated the neuroprotective effects of exercise training and/or diferuloyl methane
(DM) supplement, which is known as curcumin, on lead acetate-induced neurotoxicity in the rat hippocampus.
Sixty rats were randomly divided into six groups: 1) lead acetate, 2) DM supplement, 3) endurance training,
4) training+ DM supplement, 5) sham and 6) base. The rats in the training groups performed treadmill running
consisting of 15 to 22 m · min-1 for 25 to 64 min, 5 times a week for 8 weeks. All groups except sham received
lead acetate (20 mg · kg-1), whereas the sham group received DM solvent. In addition, the DM and training+DM
groups received DM solution (30 mg · kg-1) intraperitoneally. Chronic administration of lead acetate resulted in
a significant increase in the malondialdehyde (MDA) in plasma, but not in the hippocampus. In addition, it led
to significantly decreased brain-derived neurotrophic factor (BDNF) in the hippocampus and total antioxidant
capacity (TAC) levels, as compared to the sham group. Treadmill running, DM supplementation, or both resulted
in a significant decrease in MDA levels and significantly increased BDNF and TAC levels, as compared to the
lead acetate group. These results provide a rationale for an inhibitory role of DM supplement and regular exercise
in the attenuation of lead-induced neurotoxicity.
In the current study we investigated the neuroprotective effects of exercise training and/or diferuloyl methane
(DM) supplement, which is known as curcumin, on lead acetate-induced neurotoxicity in the rat hippocampus.
Sixty rats were randomly divided into six groups: 1) lead acetate, 2) DM supplement, 3) endurance training,
4) training+ DM supplement, 5) sham and 6) base. The rats in the training groups performed treadmill running
consisting of 15 to 22 m · min-1 for 25 to 64 min, 5 times a week for 8 weeks. All groups except sham received
lead acetate (20 mg · kg-1), whereas the sham group received DM solvent. In addition, the DM and training+DM
groups received DM solution (30 mg · kg-1) intraperitoneally. Chronic administration of lead acetate resulted in
a significant increase in the malondialdehyde (MDA) in plasma, but not in the hippocampus. In addition, it led
to significantly decreased brain-derived neurotrophic factor (BDNF) in the hippocampus and total antioxidant
capacity (TAC) levels, as compared to the sham group. Treadmill running, DM supplementation, or both resulted
in a significant decrease in MDA levels and significantly increased BDNF and TAC levels, as compared to the
lead acetate group. These results provide a rationale for an inhibitory role of DM supplement and regular exercise
in the attenuation of lead-induced neurotoxicity.
Keywords
lead, endurance exercise, diferuloyl methane supplement, BDNF, oxidative stress
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