Abstract
The present study investigated the effects of breast tumors on the blood and tissue distribution of essential trace mineral selenium (Se), and oxidative stress status of mice. Female 10-week-old BALB/cByJNarl mice were randomly assigned into control (CNL) and breast tumor-bearing (TB) groups. TB mice were injected subcutaneously into the right hind thigh with 5 × 106 EMT6 mouse mammary tumor cells. After 22 days, we measured Se concentrations, Se-dependent glutathione peroxidase (GPx) activities, and malondialdehyde (MDA) products (indicator of oxidative stress) in plasma, various tissues, and plasma vascular endothelial growth factor (VEGF) concentrations. There were no significant differences in body weights and daily intake between both groups. Compared with the CNL group, TB mice have decreases in plasma Se concentrations and GPx activities, as well as higher plasma VEGF and MDA concentrations. Plasma Se concentrations were also negatively correlated with plasma MDA and VEGF concentrations. Furthermore, tissue Se concentrations and GPx activities in TB animals were lower; whereas the MDA concentrations higher in various tissues including liver, kidney, brain, lung, spleen, and thymic tissues. In conclusion, disruption of Se homeostasis critically reflects oxidative stress in target tissues, thus may increase the risk for progression of breast cancer and metastasis.
Highlights
Breast cancer is the most commonly diagnosed cancer and the leading cause of cancer death among women worldwide [1]
The major risk factors associated with breast cancer include age, being overweight, early menarche, late menopause, first pregnancy at late age, the use of postmenopausal hormones such as estrogen and progesterone, and the presence of an inherited mutation in the BRCA1 or BRCA2 breast genes [5]
There were no significant differences in body weights (Figure 1) and average daily food intake (Table 1) between both groups throughout the experimental period (p > 0.05)
Summary
Breast cancer is the most commonly diagnosed cancer and the leading cause of cancer death among women worldwide [1]. Oxidative stress has been linked to breast cancer risk [6]. Oxidative stress causes DNA damage, which if unrepaired can lead to mutations in tumor suppressor genes [7]. Decreased Se intake status and lower toenail Se levels were associated with breast cancer risk in previous research [19,20]. The purpose of the present preliminary investigation was to examine the effects of breast tumor on the blood and tissue distribution of Se, and oxidative stress status in mice
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