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Synergistic Effects of Exercise Training and Vitamin D Supplementation on Mitochondrial Function of Cardiac Tissue, Antioxidant Capacity, and Tumor Growth in Breast Cancer in Bearing-4T1 Mice.

ABSTRACT: Both regular exercise training and vitamin D consumption are beneficial for patients with cancer. The study investigated the effects of interval exercise training (IET) or/and vitamin D supplementation on the gene expression involved in mitochondrial function of heart tissue, tumor size, and total antioxidant capacity (TAC) in breast cancer (BC) model mice. We assigned random 40 female NMRI mice to five equal groups (n = 8); the healthy control group (H.C), cancer control group (Ca.C), cancer with the vitamin D group (Ca.VD), cancer exercise group (Ca.Ex), and cancer exercise along with the vitamin D group (Ca.Ex.VD). Forty-eight hours after treatment, we anesthetized the animals and performed the isolation of heart tissue and blood serum for further studies. The results showed that the lowest mean body weight at the end of the treatments was related to Ca.C (p = 0.001). Vitamin D treatment alone has increased tumor volume growth by approximately 23%; in contrast, co-treatment with exercise and vitamin D inhibited tumor growth in mice (P = 0.001), compared with the cancer control (12%). TAC levels were higher in the group that received both vitamin D and exercise training (Ca.Ex.VD) than in the other treatment groups (Ca.VD and Ca.Ex) (p = 0.001). In cardiac tissue, vitamin D treatment induces an elevation significantly of the mRNA expression of Pgc1-α, Mfn-1, and Drp-1 genes (p = 0.001). The study has shown the overexpression of vitamin D in female mice, and synergistic effects of IET with vitamin D on weight loss controlling, antitumorigenesis, improvement of antioxidant defense, and the modulation of gene expression. The synergistic responses were likely by increasing mitochondrial fusion and TAC to control oxidative stress. We recommended being conducted further studies on mitochondrial dynamics and biogenesis focusing on risk factors of cardiovascular disease (CVD) in patients with BC.

SUBMITTER: Jafari A

PROVIDER: S-EPMC8076802 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The molecular mechanisms of exercise-induced cardiovascular protection are poorly understood. There is growing evidence that reactive oxygen species (ROS) are necessary for some of these adaptations and antioxidants may be used to investigate this effect. This study aimed to determine the effects of exercise and/or antioxidant supplementation on myocardial and vascular endothelium gene expression. Male Wistar rats were divided into four groups: i) endurance exercise (90min of treadmill running 4d/week, 14 weeks); ii) antioxidant-treated; iii) antioxidant and endurance exercise and iv) control. The supplemented animals received Vitamin E (1000 IU/kg diet) and ï¡-lipoic acid (1.6 g/kg diet) mixed with rat chow. cDNA microarray analysis was performed using purified endothelial RNA from myocardial and coronary artery endothelial cells and showed that the expression levels of 35, 40 and 40 genes were altered for groups i, ii, and iii respectively compared to control. Differentially expressed genes were analysed using the KEGG pathway database, hierarchical cluster and DAVID analysis. These analyses revealed that a gene involved in cardiovascular disease progression, Ras homolog gene family member A (RhoA) was down-regulated by exercise, upregulated by antioxidant supplementation and the combination of exercise and antioxidant blunted both effects. These findings were confirmed by real-time PCR. In summary, exercise and antioxidant supplementation affect endothelial cell gene expression and ROS appear necessary for some of these adaptations. 48 Male Wistar rats were divided into four groups: i) endurance exercise (90min of treadmill running 4d/week, 14 weeks); ii) antioxidant-treated; iii) antioxidant and endurance exercise and iv) control. The supplemented animals received Vitamin E (1000 IU/kg diet) and ï¡-lipoic acid (1.6 g/kg diet) mixed with rat chow. cDNA microarray analysis was performed using purified endothelial RNA from myocardial and coronary artery endothelial cells. Based on the limited material available, it was necessary to combine the RNA into three pools per treatment group for CAEC (approx 400 ng of total RNA), and four pools for LVEC (approx 1 Î¼g of total RNA) with an additional reference pool from each control group.

Project description:BackgroundCardiac troponin is the biochemical gold standard to diagnose acute myocardial infarction. Interestingly however, elevated cardiac troponin concentrations are also frequently observed during and after endurance-type exercise. Oxidative stress associated with prolonged exercise has been proposed to contribute to cardiac troponin release. Therefore, the aim of this study was to assess the effect of 4 week astaxanthin supplementation (a potent cartenoid antioxidant) on antioxidant capacity and exercise-induced cardiac troponin release in cyclists.MethodsThirty-two well-trained male cyclists (age 25±5, weight 73±7 kg, maximum O2 uptake 60±5 mL·kg(-1)·min(-1), Wmax 5.4±0.5 W·kg(-1); mean ± SD) were repeatedly subjected to a laboratory based standardized exercise protocol before and after 4 weeks of astaxanthin (20 mg/day), or placebo supplementation in a double-blind randomized manner. Blood samples were obtained at baseline, at 60 min of cycling and immediately post-exercise (≈ 120 min).ResultsThe pre-supplementation cycling trial induced a significant rise of median cardiac troponin T concentrations from 3.2 (IQR 3.0-4.2) to 4.7 ng/L (IQR 3.7-6.7), immediately post-exercise (p<0.001). Four weeks of astaxanthin supplementation significantly increased mean basal plasma astaxanthin concentrations from non-detectable values to 175±86 µg·kg(-1). However, daily astaxanthin supplementation had no effect on exercise-induced cardiac troponin T release (p = 0.24), as measured by the incremental area under the curve. Furthermore, the elevation in basal plasma astaxanthin concentrations was not reflected in changes in antioxidant capacity markers (trolox equivalent antioxidant capacity, uric acid, and malondialdehyde). Markers of inflammation (high-sensitivity C-reactive protein) and exercise-induced skeletal muscle damage (creatine kinase) were equally unaffected by astaxanthin supplementation.ConclusionDespite substantial increases in plasma astaxanthin concentrations, astaxanthin supplementation did not improve antioxidant capacity in well-trained cyclists. Accordingly, exercise-induced cardiac troponin T concentrations were not affected by astaxanthin supplementation.Trial registrationClinicalTrials.gov NCT01241877.

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Synergistic Effects of Exercise Training and Vitamin D Supplementation on Mitochondrial Function of Cardiac Tissue, Antioxidant Capacity, and Tumor Growth in Breast Cancer in Bearing-4T1 Mice.

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