Increased xanthine oxidase-related ROS production and TRPV1 synthesis preceding DOMS post-eccentric exercise in rats

Retamoso, Leandro Thies; Silveira, Mauro Eduardo Porto da; Lima, Frederico Diniz; Busanello, Guilherme L.; Bresciani, Guilherme; Ribeiro, Leandro Rodrigo; Chagas, Pietro Maria; Nogueira, Cristina W.; Braga, Ana Cláudia Monteiro; Furian, Ana Flávia; Oliveira, Mauro Schneider; Fighera, Michele Rechia; Royes, Luiz Fernando Freire

doi:10.1016/j.lfs.2016.03.029

Cited by 19 publications

(16 citation statements)

References 60 publications

(74 reference statements)

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“…Our resistance exercise protocol was suitable to increase oxidative stress as assessed by lipoperoxidation levels in muscle, corroborating previous data about resistance exercise [ 14 – 17 , 22 ]. A decreased oxidative stress in muscles irradiated with 4J energy demonstrates to be of interest, in which more positive results were noticed for analyses of lipid peroxidation performed immediately after RE bout.…”

Section: Discussionsupporting

confidence: 87%

“…An excessive increase of the oxidative stress during muscle work can cause damage to proteins and cellular dysfunction. Moreover, high-intensity exercises (e.g., upward of the second ventilatory threshold) are marked by decompensated metabolic acidosis and sarcolemma microinjury, which can lead to inflammation and a burst of free radicals [ 17 , 18 ]. The implication of these findings is a delayed postexercise muscle recovery, hence, impairing the quality of training sessions [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

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Photobiomodulation Leads to Reduced Oxidative Stress in Rats Submitted to High-Intensity Resistive Exercise

Oliveira

Antônio

Arsa

et al. 2018

Oxidative Medicine and Cellular Longevity

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The aim of this study was to determine whether oxidative stress markers are influenced by low-intensity laser therapy (LLLT) in rats subjected to a high-intensity resistive exercise session (RE). Female Wistar rats divided into three experimental groups (Ctr: control, 4J: LLLT, and RE) and subdivided based on the sampling times (instantly or 24 h postexercise) underwent irradiation with LLLT using three-point transcutaneous method on the hind legs, which was applied to the gastrocnemius muscle at the distal, medial, and proximal points. Laser (4J) or placebo (device off) were carried out 60 sec prior to RE that consisted of four climbs bearing the maximum load with a 2 min time interval between each climb. Lipoperoxidation levels and antioxidant capacity were obtained in muscle. Lipoperoxidation levels were increased (4-HNE and CL markers) instantly post-RE. LLLT prior to RE avoided the increase of the lipid peroxidation levels. Similar results were also notified for oxidation protein assays. The GPx and FRAP activities did not reduce instantly or 24 h after RE. SOD increased 24 h after RE, while CAT activity did not change with RE or LLLT. In conclusion, LLLT prior to RE reduced the oxidative stress markers, as well as, avoided reduction, and still increased the antioxidant capacity.

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Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Photobiomodulation Leads to Reduced Oxidative Stress in Rats Submitted to High-Intensity Resistive Exercise

Oliveira

Antônio

Arsa

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…Oxidative stress-mediated lipid peroxidation also denatures cellular proteins and DNA resulting in loss of membrane integrity. Consequently, cardiac enzymes such as LDH and CK-MB are released from the intracellular compartment to the extracellular fluid [ 36 , 37 ]. In our study, we observed that cardiac enzyme levels were raised in the IR-control group.…”

Section: Discussionmentioning

confidence: 99%

“…The apoptosis-induced cardiac damage following IR is halted by the activation of ERK1/ERK2 [ 43 ]. There is substantial evidence regarding improvement of cardiac function following IR injury by suppressing cardiomyocyte apoptosis through targeted inhibition of p38 MAPK [ 36 , 39 , 44 ]. The present study findings reveal for the first time that febuxostat modulates the MAPK in the heart tissue as evidenced by enhanced activities of ERK1/ERK2, increased Bcl-2, decreased Bax, reduced caspase-3, and fewer DNA fragments in febuxostat-treated groups relative to the untreated group.…”

Section: Discussionmentioning

confidence: 99%

Febuxostat Modulates MAPK/NF-κBp65/TNF-α Signaling in Cardiac Ischemia-Reperfusion Injury

Khan

Malhotra

Rani

et al. 2017

Oxidative Medicine and Cellular Longevity

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Xanthine oxidase and xanthine dehydrogenase have been implicated in producing myocardial damage following reperfusion of an occluded coronary artery. We investigated and compared the effect of febuxostat and allopurinol in an experimental model of ischemia-reperfusion (IR) injury with a focus on the signaling pathways involved. Male Wistar rats were orally administered vehicle (CMC) once daily (sham and IR + control), febuxostat (10 mg/kg/day; FEB10 + IR), or allopurinol (100 mg/kg/day; ALL100 + IR) for 14 days. On the 15th day, the IR-control and treatment groups were subjected to one-stage left anterior descending (LAD) coronary artery ligation for 45 minutes followed by a 60-minute reperfusion. Febuxostat and allopurinol pretreatment significantly improved cardiac function and maintained morphological alterations. They also attenuated oxidative stress and apoptosis by suppressing the expression of proapoptotic proteins (Bax and caspase-3), reducing TUNEL-positive cells, and increasing the level of antiapoptotic proteins (Bcl-2). The MAPK-based molecular mechanism revealed suppression of active JNK and p38 proteins concomitant with the rise in ERK1/ERK2, a prosurvival kinase. Additionally, a reduction in the level of inflammatory markers (TNF-α, IL-6, and NF-κB) was also observed. The changes observed with febuxostat were remarkable in comparison with those observed with allopurinol. Febuxostat protects relatively better against IR injury than allopurinol by suppressing inflammation and apoptosis mediating the MAPK/NF-κBp65/TNF-α pathway.

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“…In addition, resistance exercise can also evoke increased free radical production in muscle because of the occurrence of intermittent bouts of hypoxia/reperfusion. An excessive increase in oxidative stress or a free radical burst in working muscles can override the physiological benefits of exercise causing extensive damage to proteins and cellular dysfunction [ 7 , 8 ]. This is a key concern during intense training stages, in which the burst in free radicals can overcome the existing antioxidant mechanisms.…”

mentioning

confidence: 99%

Oxidative Stress in Muscle Diseases: Current and Future Therapy

Serra

Prokić

Vasconsuelo

et al. 2018

Oxidative Medicine and Cellular Longevity

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Increased xanthine oxidase-related ROS production and TRPV1 synthesis preceding DOMS post-eccentric exercise in rats

Cited by 19 publications

References 60 publications

Photobiomodulation Leads to Reduced Oxidative Stress in Rats Submitted to High-Intensity Resistive Exercise

Photobiomodulation Leads to Reduced Oxidative Stress in Rats Submitted to High-Intensity Resistive Exercise

Febuxostat Modulates MAPK/NF-κBp65/TNF-α Signaling in Cardiac Ischemia-Reperfusion Injury

Oxidative Stress in Muscle Diseases: Current and Future Therapy

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