Acute Effects of Moderate and Strenuous Running on Trace Element Distribution in the Brain, Liver, and Spleen of Trained Rats

Ergen, Kıvanç; Ínce, Hürrem; Düzova, Halil; Karakoç, Yunus; Emre, Memet Hanifi

doi:10.5152/balkanmedj.2012.093

Cited by 9 publications

(4 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…At the same time, no significant group difference was detected in other tissues including skeletal and cardiac muscle, liver, and hair . These data correspond to the study by Ergen et al (2013) who demonstrated that strenuous exercise resulted in a significant decrease in frontal lobe, liver, and spleen Co levels, whereas moderate exercise reduced metal levels in brain stem, liver, and spleen (Ergen et al, 2013). Hepatic Co levels were also reduced in rats exposed to strenuous swimming exercise (Sivrikaya et al, 2013).…”

Section: Cobalt Status In Athletessupporting

confidence: 89%

Cobalt in athletes: hypoxia and doping - new crossroads

Skalny¹,

Zaitseva²,

Gluhcheva³

et al. 2019

J Appl Biomed

View full text Add to dashboard Cite

Cobalt is an essential trace element that is known to mimic hypoxia and hypoxic training. Inorganic Co compounds are capable of Hypoxiainducible factor-1 (HIF-1) activation, resulting in up-regulation of gene expression including erythropoietin (Epo). Experimental studies have demonstrated that Co treatment may increase hypoxic tolerance of different tissues, improve muscle metabolism and exercise performance. Other mechanisms may also involve modulation of steroid hormone and iron metabolism. Based on these experimental studies, in 2017 inorganic cobalt compounds were added into the World Anti-Doping Agency (WADA) prohibited list as doping agents. However, the existing data on beneficial effects of cobalt on exercise performance in athletes are scarce. Similarly, only experimental studies demonstrated exercise-induced decrease in tissue Co levels, whereas human data are inconsistent. In addition, multiple studies have demonstrated that excessive Co intake may be toxic due to prooxidant, proinflammatory, and proapoptotic activity. Therefore, monitoring of Co deficiency and overload is required to prevent potential health hazards in athletes. At the same time, modulation of Co status should be performed through supplementation avoiding excessive doses of inorganic cobalt that are used for doping and are accompanied by adverse health effects of metal toxicity.

show abstract

Section: Cobalt Status In Athletessupporting

confidence: 89%

Cobalt in athletes: hypoxia and doping - new crossroads

Skalny¹,

Zaitseva²,

Gluhcheva³

et al. 2019

J Appl Biomed

View full text Add to dashboard Cite

show abstract

“…for 28 consecutive days. Higher Cr residues were detected in the brain homogenate tissues of the Cr-intoxicated group compared to the unexposed animals, indicating the ability of Cr to accumulate in the brain tissues and trigger neurotoxicity [ 41 ]. On the other hand, SA was shown to alter the biodistribution of Cr (VI) and reduce its levels in brain tissues, as evidenced by the notable reduction in the Cr level in the brain tissues of Group IV (Cr+SA) compared to the Cr-intoxicated group.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of sodium alginate against chromium-induced brain damage in rats

2022

View full text Add to dashboard Cite

Oral exposure to chromium hexavalent [Cr(VI)] has disastrous impacts and affects many people worldwide. Cr(VI) triggers neurotoxicity via its high oxidation potential by generating high amount of ROS. Meanwhile, alginates are known by their chelating activity and ability to bind heavy metals and toxins, in addition to their antioxidant, anti-inflammatory, and anti-apoptotic activities. So, this study aimed to explore the neuroprotective potential of sodium alginate (SA) against cellular injury, DNA damage, macromolecule alterations, and apoptosis induced by oral ingestion of Cr. Forty Wistar male rats were divided into 4 groups; group I: standard control ingested with the vehicle solution, group II: Cr-intoxicated group received 10 mg/kg b.w. of potassium dichromate orally by gavage and kept without treatment, group III: SA group in which rats were orally exposed to 200 mg/kg b.w. of SA only, and group IV: SA-treated group that received 200 mg/kg b.w. of SA along with Cr for 28 consecutive days. Neurotransmitters such as Acetyl choline esterase (AchE), Monoamine oxidase A (MAOA) concentrations, Dopamine (DA) and 5-Hydroxytryptamine (5-HT) levels were assessed in brain homogenate tissues. Neurobiochemical markers; NAD+ and S100B protein were investigated in the brain tissues and serum, respectively. Levels of HSP70, caspase-3, protein profiling were evaluated. DNA damage was determined using the Comet assay. Results revealed a significant reduction in the AchE and MAOA concentrations, DA, 5-HT, and NAD+ levels, with an increase in the S100B protein levels. Cr(VI) altered protein pattern and caused DNA damage. High levels of HSP70 and caspase-3 proteins were observed. Fortunately, oral administration of SA prevented the accumulation of Cr in brain homogenates and significantly improved all investigated parameters. SA attenuated the ROS production and relieved the oxidative stress by its active constituents. SA can protect against cellular and DNA damage and limit apoptosis. SA could be a promising neuroprotective agent against Cr(VI)-inducing toxicity.

show abstract

“…In a study of chromium (VI) stress, a twofold increase in brain Mn levels accompanied increased Cr concentrations (75). Metabolic stress may alter Mn distribution in tissues, as suggested by a recent study that found decreased levels of Mn in the brain stem and frontal lobe after strenuous exercise relative to control conditions and moderate exercise (83). Dietary iron levels may have an impact on levels of Mn accumulation in the brain (96).…”

Section: Manganese Distribution and Concentrations In The Central Nermentioning

confidence: 99%

Manganese Is Essential for Neuronal Health

et al. 2015

View full text Add to dashboard Cite

The understanding of manganese (Mn) biology, in particular its cellular regulation and role in neurological disease, is an area of expanding interest. Mn is an essential micronutrient that is required for the activity of a diverse set of enzymatic proteins (e.g., arginase and glutamine synthase). Although necessary for life, Mn is toxic in excess. Thus, maintaining appropriate levels of intracellular Mn is critical. Unlike other essential metals, cell-level homeostatic mechanisms of Mn have not been identified. In this review, we discuss common forms of Mn exposure, absorption, and transport via regulated uptake/exchange at the gut and blood-brain barrier and via biliary excretion. We present the current understanding of cellular uptake and efflux as well as subcellular storage and transport of Mn. In addition, we highlight the Mn-dependent and Mn-responsive pathways implicated in the growing evidence of its role in Parkinson's disease and Huntington's disease. We conclude with suggestions for future focuses of Mn health-related research.

show abstract

Acute Effects of Moderate and Strenuous Running on Trace Element Distribution in the Brain, Liver, and Spleen of Trained Rats

Cited by 9 publications

References 32 publications

Cobalt in athletes: hypoxia and doping - new crossroads

Cobalt in athletes: hypoxia and doping - new crossroads

Neuroprotective effect of sodium alginate against chromium-induced brain damage in rats

Manganese Is Essential for Neuronal Health

Contact Info

Product

Resources

About