Selenium By: Danielle Roller

What Is Selenium? Trace Mineral Essential in good health Small amounts micrograms Selenoproteins = antioxidant enzymes

Selenium Sources Amount in food depends on amount in the soil Nuts Fish Beef Chicken Turkey Grains Eggs 6 whole nuts (1 oz)= 544 mcg

What About Selenium? Improves brain function: protects brain cells Inhibit genetic damage Anti-viral Anti Heart Disease & Anti-Diabetes: Deficiency  Keshan Disease in China Proteins provide antioxidant effects  Male fertility  Anti asthma, arthritis, muscular  Thyroid functiondystrophy & cystic fibrosis  Supports immune function  Reduces cancer risk  Anti-aging Zeng, Huawei (2009)

“What is the relationship between selenium & cancer?”

Types Of Cancers Breast Colon Head Prostate Lymphatic Neck Lung Zeng, Huawei (2009)

Cancer Prevention “ANTI-TUMORIGENIC” Vitamin C, E & beta carotene Antioxidant Cofactor to scavenge free radicals (cancer and chemotherapy) Glutathione peroxidase enzyme Cell Apoptosis Zeng, Huawei (2009)

Defining the optimal selenium dose for prostate cancer risk reduction: insights from the u-shaped relationship between selenium status, DNA damage, and apoptosis Bostwick, D., Chiang,E., Combos, G., Kengeri, S., Morris, S., Shen, S., Waters, D. and Xu, H.

Objective To provide further research based on the dietary intake of selenium providing a decreased risk in the onset of prostate cancer

Study Design Experimental Study 69 male beagle dogs 7 months control & experimental

Methods Control group (n=20): Nutritionally adequate with selenium from the start and was fed a adequate selenium diet. Experimental group (n=29): Nutritionally adequate with selenium but received daily supplemetation – 3 mcg/kg/day – 6 mcg/kg/day Once 7 months complete – Low = <6.7 ppm – Medium = ppm – High = >0.92 ppm Observed “hot spots” (cells that went through apoptosis) Rate of DNA damage in the cells of the prostate.

Descriptive Statistics Range Mean apoptotic index Median

Inferential Statistics 95% confidence interval Odds Ratio Multivariate analysis Chi-Square T-test

Results Moderate Selenium Status Less DNA damage by 84% 4.1x more apoptotic “hot spots” Selenium exposure = positive outcome Normal Distribution Curve

Low & High Selenium Status  Slight increase in epithelial cell apoptosis  More DNA Damage  Selenium supplementation was not beneficial

Selenium status vs. epithelial cell apoptosis

Strengths Population used Clear evidence of planning and organization in methods Internal Validity: Confounding Variables Suggestions of further research In vivo Study

Weaknesses In vivo Sample size of population used External Validity Not clear which group received selenium supplementation (How much?)

Support Reduces cancer risks by halting damaged DNA molecules from reproducing (cell growth) * Inducing apoptosis - “hot spots” Prevents tumors from developing Slows cancer progression in patients who already have it Zeng, Huawei (2009)

Selenium substitution during radiotherapy of solid tumors Bruns, F., Buntzel, J., Glatzel, M., Kisters, K., Kundt, C., Micke, O., Mucke, R., Schafer, U., and Schanekaes, K.

What is the relationship between selenium and cancer?

Chemotherapy Treatment involving the use of chemical agents to stop cancer cells from growing Increases free radicals because of toxic drugs involved in the process Increases amount of damaged DNA

Objective Determining what the sufficient selenium dose is in supportive therapy.

Study Design Experimental study 81 gynecological cancer patients 48 head and neck cancer patients Control & Experimental Group

Methods Group 1(Experimental)  500 micrograms SE Group 2 (Control)  Received no Se supplementation Blood samples collected before, half way through, after, and 6 weeks after radiotherapy Results sent to laboratory

Descriptive statistics Mean Standard Error P-value

Inferential statistics Leven’s test T-test Chi-Square test Fisher’s exact test Mann-Whitney u-test

Results No differences with location of tumors Mann-Whitney u-test  50% significant differences in Se concentrations in the blood at the end of radiotherapy (p<0.001) No significant difference between groups before and 6 weeks after

Selenium concentrations (whole blood) during radiotherapy Büntzel, J (2010)

Additional Results Se provided as therapeutic option GYN:  diarrheas Head & Neck: improved loss of taste &  “dysphagia” Both trials showed clinical effects with toxicity of anti-cancer treatments 500 microgram dose  blood concentrations after 3 weeks Se dose either increased more or started earlier (10-15 weeks prior) to have earlier effects in reducing toxicity during first part of radiotherapy.

Strengths Accepted their hypothesis Evidence of planning & organization Research Questions (Objective) clearly stated Internal validity: Chance Population used

Weaknesses Internal Validity: confounding variables

Support Blocks chemical reactions that produce free radicals  gluthione peroxidase enzyme recognition of DNA damage   DNA repair & DNA repair synthesis. Minimizing potential damage to normal cells from free radicals Enhancing effectiveness of radiation process by 3.)  toxicity of chemotherapy drugs 4.) Therapy = “selective toxin” Büntzel, J. (2010)