**6. Selenium and prostate cancer**

Selenium (Se) is a natural nutrient which can be found in different types of food. The human body utilizes a trace amount of this mineral in order to function optimally. It is reported to have powerful antioxidant properties which prevent and reduce oxidative stress. Selenium is an essential micronutrient that functions as a redox gatekeeper through its incorporation into proteins to alleviate oxidative stress in cells [95]. It also plays a crucial role in development and a wide variety of other physiological processes including effect immune responses, metabolism, and thyroid function [96, 97]. This has been attributed to selenium's ability to reduce DNA damage and oxidative stress, boost the immune system, and destroy cancer cells. The nutritional status of this metalloid has been difficult to assess via food intake data alone because many factors influence its presence in the food chain [98]. Regular adult intakes of at least 40 μg/day are required to support the maximal expression of the selenium enzymes, and perhaps as much as 300 μg/day to reduce risks of cancer is needed [99].

A number of randomized intervention trials and epidemiological studies suggest that prostate cancer risk may be decreased by selenium intake [100–105]. Studies from 2008 to 2014 (**Table 3**) have shown that selenium supplementation may have some level of a protective role against prostate cancer. In the Nutritional Prevention Cancer Study (a multicenter, double-blind, randomized, placebo-controlled cancer

**229**

supplementations.

disease [106].

**Table 3.**

*Dietary Antioxidants in the Chemoprevention of Prostate Cancer*

**study**

Lippman et al. [132] 2009 Sel. Sup 1.04 0.90–1.18 4% Dunn et al. [133] 2010 Sel. Sup 1.04 0.87–1.24 4% Marshall et al. [134] 2011 Sel. Sup 1.09 0.93–1.27 9% Klein et al. [16] 2011 Sel. Sup 0.90 0.93–1.27 10% Algatar et al. [135] 2013 Sel. Sup 0.90 0.48–1.70 10% Kristal et al. [42] 2014 Sel. Sup 1.25 0.79–1.98 25%

Peters et al. [104] 2008 Sel. Sup 0.90 0.62–1.30 10% Chan et al. [105] 2009 Plasma 1.35 0.99–1.84 35% Geybels et al. [112] 2013 Nail 0.37 0.27–0.51 63%

Allen et al. [136] 2008 Plasma 0.96 0.07–1.31 4%

Gill et al. [138] 2009 Serum 0.82 0.59–1.14 18% Zhang et al. [139] 2009 Diet 1.30 0.30–5.70 30% Outzen et al. [108] 2016 Plasma 1.01 0.94–1.08 1%

2008 Serum 0.16 0.06–0.49 84%

**Sample RR 95% CI P.R.E** 

**outcome**

prevention trial), oral selenium supplementation (200 μg of selenium per day) lowers the incidence of prostate cancer (RR 0.37, 95% CI: 0.18–0.71, P = 0.02) [106]. Follow-up from this study reported 2 years later found that selenium supplementation reduced the incidence of localized and also advanced prostate cancer

*RR = relative risk, CI = confidence interval, P.R.E = percentage relative effect, Sel. Sup = selenium supplement.*

In the selenium and vitamin E cancer prevention trial (SELECT), there was decrease in prostate cancer risk with either vitamin E or selenium supplements [107]. In a follow-up from this study, there was an absolute elevation of the risk of prostate cancer (per 1000 person-years) that was 0.8 for selenium, 1.6 for vitamin E, and 0.4 for the combination [16]. Chan and colleagues conducted a case-cohort study of participants in SELECT, randomized to placebo, vitamin E and selenium. They reported that selenium- or vitamin E variants may influence the overall and high-grade risk of prostate cancer and could possibly modify the patient's response to either selenium or vitamin E supplementation [28]. Furthermore, from the SELECT trial involving a stratified case-cohort sample of incident prostate cancer cases, elevated high-grade prostate cancer risk was observed in men supplemented with high-dose alpha-tocopherol and selenium, possibly due to interaction between selenium (or selenomethionine) and alpha-tocopherol [41]. The results of the SELECT study showed that it failed to demonstrate any significant decrease in prostate cancer ascribable vitamin E and selenium

Researchers found it useful to investigate any possible association between plasma selenium levels and prostate cancer risk. In the case-control study by Brooks et al., low plasma selenium levels were associated with a four- to fivefold

*DOI: http://dx.doi.org/10.5772/intechopen.85770*

**Method Name of author(s) Year of** 

Pourmand et al. [137]

*Showing studies on the effect of selenium on prostate cancer.*

Random control trials

Cohort

Case-control


#### *Dietary Antioxidants in the Chemoprevention of Prostate Cancer DOI: http://dx.doi.org/10.5772/intechopen.85770*

#### **Table 3.**

*Antioxidants*

in eliminating cancer cells. Further investigations proved that polyphenols employ biological methods in providing cancer prevention and even elimination, such as binding to multiple cellular proteins and regulating signal transduction. Alterations in signal pathways affect multiple processes that hinder cancer initiation, progression, and metastasis [89]. Among green tea catechins, epigallocatechin-3-gallate (EGCG) is widely investigated for its cancer preventive properties. In a recent study, the difluoro analog, called (-)-5,7-difluoro-epicatechin-3-O-gallate and (-)-epicatechin-3-O-gallate from green tea dose-dependently, inhibits tumorigenesis during initiation, promotion, and progression in low-metastatic LNCaP and high-metastatic PC-3 prostate cancer cells [90]. There is also recent evidence that green tea catechins contribute to the inhibition of prostate carcinogenesis by modifying miRNA expression and their target mRNAs, as well as acting as epigenetic modulators [91]. Epicatechin-3-O-gallate and theaflavins have been found to reduce the rate of cell growth in DU 145 human prostate cancer cells [92]. The inhibition of proliferation in the human prostate cancer DU145 cells by tea polyphenols may be

associated with reduction in the expression of the surviving gene [93].

deacetylase, irrespective of their p53 status [6].

**6. Selenium and prostate cancer**

risks of cancer is needed [99].

The extensive methylation of green tea polyphenols and low bioavailability limits their chemopreventive activity. A combination of green tea polyphenols and a methylation inhibitor quercetin inhibit growth and proliferation in androgensensitive LAPC-4 prostate cancer cells. There was also evidence of stimulation of apoptosis and inhibition of phosphatidylinositol 3-kinase/Akt signaling [14]. More in-depth studies have demonstrated that green tea polyphenols induced p53-dependent and p53-independent apoptosis in human prostate cancer LNCaP cells by two distinct pathways. One pathway involved the inhibition of the survival pathway where there is Akt deactivation and loss of BAD phosphorylation, while in the other, there is FAS upregulation via activation of c-jun-N-terminal kinase resulted in caspase-8 activation, FADD phosphorylation, and truncation of BID [94]. There is documentation of other molecular mechanisms by which green tea polyphenols trigger death and apoptosis of human prostate cancer cells via inhibition histone

Selenium (Se) is a natural nutrient which can be found in different types of food. The human body utilizes a trace amount of this mineral in order to function optimally. It is reported to have powerful antioxidant properties which prevent and reduce oxidative stress. Selenium is an essential micronutrient that functions as a redox gatekeeper through its incorporation into proteins to alleviate oxidative stress in cells [95]. It also plays a crucial role in development and a wide variety of other physiological processes including effect immune responses, metabolism, and thyroid function [96, 97]. This has been attributed to selenium's ability to reduce DNA damage and oxidative stress, boost the immune system, and destroy cancer cells. The nutritional status of this metalloid has been difficult to assess via food intake data alone because many factors influence its presence in the food chain [98]. Regular adult intakes of at least 40 μg/day are required to support the maximal expression of the selenium enzymes, and perhaps as much as 300 μg/day to reduce

A number of randomized intervention trials and epidemiological studies suggest that prostate cancer risk may be decreased by selenium intake [100–105]. Studies from 2008 to 2014 (**Table 3**) have shown that selenium supplementation may have some level of a protective role against prostate cancer. In the Nutritional Prevention Cancer Study (a multicenter, double-blind, randomized, placebo-controlled cancer

**228**

*Showing studies on the effect of selenium on prostate cancer.*

prevention trial), oral selenium supplementation (200 μg of selenium per day) lowers the incidence of prostate cancer (RR 0.37, 95% CI: 0.18–0.71, P = 0.02) [106]. Follow-up from this study reported 2 years later found that selenium supplementation reduced the incidence of localized and also advanced prostate cancer disease [106].

In the selenium and vitamin E cancer prevention trial (SELECT), there was decrease in prostate cancer risk with either vitamin E or selenium supplements [107]. In a follow-up from this study, there was an absolute elevation of the risk of prostate cancer (per 1000 person-years) that was 0.8 for selenium, 1.6 for vitamin E, and 0.4 for the combination [16]. Chan and colleagues conducted a case-cohort study of participants in SELECT, randomized to placebo, vitamin E and selenium. They reported that selenium- or vitamin E variants may influence the overall and high-grade risk of prostate cancer and could possibly modify the patient's response to either selenium or vitamin E supplementation [28]. Furthermore, from the SELECT trial involving a stratified case-cohort sample of incident prostate cancer cases, elevated high-grade prostate cancer risk was observed in men supplemented with high-dose alpha-tocopherol and selenium, possibly due to interaction between selenium (or selenomethionine) and alpha-tocopherol [41]. The results of the SELECT study showed that it failed to demonstrate any significant decrease in prostate cancer ascribable vitamin E and selenium supplementations.

Researchers found it useful to investigate any possible association between plasma selenium levels and prostate cancer risk. In the case-control study by Brooks et al., low plasma selenium levels were associated with a four- to fivefold elevated risk of prostate cancer [101]. In a retrospective cohort study, higher levels of selenium were associated with decreased risk of aggressive prostate cancer (RR 0.60, 95% CI: 0.32–1.12), and the relationship at diagnosis may be modified by the manganese superoxide dismutase (SOD2) gene [105]. Furthermore, in a study involving the Within the Danish "Diet, Cancer and Health" cohort, higher levels of plasma selenium were not associated with lower risk of high-grade prostate cancer disease or prostate cancer-specific mortality [108]. A systematic review and metaanalysis of case-control studies, randomized controlled trials, and prospective cohort studies showed decreased prostate cancer risk with increasing serum/plasma selenium levels (up to 170 ng/ml) when 12 studies were analyzed and also lower risk of disease with toenail selenium levels between 0.85 and 0.94 μg/g (estimated RR 0.29, 95% CI: 0.14–0.61) in three high-quality studies [109]. Therefore, although there is evidence of a potential protective effect of selenium in terms of its status and supplementation, further studies are required especially in low-selenium status populations.

In the last 10 years, a number of systematic and meta-analysis have been conducted to examine the relationship between selenium status and prostate cancer. In one study reported by Sayehmirj and colleagues, the relative risks for prostate cancer (based on case-control, cohort, and randomized control trials) on serum and nail samples were 0.85 (95% CI: 0.61–1.17) and 0.66 (95% CI: 0.41–1.05), respectively. They also reported a relative risk of 0.67 (95% CI: 0.52–0.87) between selenium levels and advanced prostate cancer [110]. The authors concluded that selenium supplementation could have a protective role against the initiation and progression to advanced stages [110]. A MOOSE-compliant meta-analysis of 17 studies showed a significant inverse association between prostate cancer risk and serum selenium levels (RR 0.76, 95% CI: 0.64–0.76) [82].

Even though these studies suggest that higher levels of selenium are associated with decreased risk of prostate cancer; there are others that have demonstrated otherwise. An analysis of 15 prospective studies by Allen et al. failed to show any association between blood selenium levels and risk of prostate cancer (OR, 1.01, 95% CI: 0.83–1.23). However, high blood selenium levels were not associated with nonaggressive disease, but with aggressive disease (OR 0.43, 95% CI: 0.21–0.87) [111]. Another key finding in this study was that nail selenium levels were significantly inversely associated with prostate cancer risk (OR0.29, 95% CI: 0.22–0.40, P < 0.001) and also with both aggressive and nonaggressive disease [111]. Similarly, in the prospective Netherlands cohort study, toenail selenium levels were associated with a significant reduction in the risk of advanced prostate cancer (RR 0.37, 95% CI: 0.27–0.51; P < 0.001) [112]. However, in a case-control study, selenium levels in toenail were not associated with prostate cancer risk, and its supplementation while not having any effect among participants with low selenium status elevates the risk (by 91%, P = 0.07) among those with higher selenium status [42]. The authors suggest that men with low selenium status did not benefit from its supplementation which increased the risk of high-grade prostate cancer among those participants with high selenium status [42].

The effects of selenium on prostate cancer remain uncertain. In a prospective cohort study in the United States, reported by Peter et al., showed that long-term selenium supplementation did not lower the overall risk of prostate cancer (HR 0.90, 95% CI: 0.62–1.3) with participants having an average intake of >50 μg/day over a 10-year period [104]. In a Cochrane review including randomized controlled trials and longitudinal observational studies, there was no association between selenium supplementation and the risk of prostate cancer [113], nor in a Mendelian randomization analysis by Yarmolinsky et al. where the authors suggested that selenium supplementation could have unfavorable effects on risks of advanced disease

**231**

*Dietary Antioxidants in the Chemoprevention of Prostate Cancer*

[114]. There is further supporting evidence in the follow-up of the Procomb trial where there was no association between selenium supplementation and prostate cancer risk [115]. Conversely, there are studies that suggest caution with selenium supplement usage among males with prostate cancer. In the Health Professionals Follow-Up Study (over a 22-year period) of men diagnosed with nonmetastatic prostate cancer, supplementation of 140 or more μg/day of selenium had a 2.6-fold risk of prostate cancer mortality (95% CI: 1.44–4.70, P = 0.001) compared with

The mechanism of action of selenium in the inhibition of cancer development could include reduction in DNA damage. Waters et al. reported that dietary supplementation of selenium increases epithelial cell apoptosis in prostate and DNA

Vitamin C is mainly obtained from vegetables and fruit sources and is considered to be a very important water-soluble antioxidant [118]. Foods and supplements are sources, which provide vitamin C intake while that from foods only is referred to as dietary vitamin C. There is evidence that the mechanisms by which vitamin C prevents the harmful effects of carcinogens include decreasing oxidative DNA damage [119, 120]. Vitamin C functions as a scavenger of free radicals and, therefore, has a potential role in the chemoprevention of prostate cancer [121]. Animal and *in vitro* studies have demonstrated that it could inhibit the cell growth and viability [8]. Menon and colleagues suggested that vitamin C may be a potent anticancer agent as it inhibits tumor growth by producing reactive oxygen species [122]. In another study, vitamin C inhibits cell growth and division via the generation of

A number of epidemiological studies have documented the relationship between

risk of prostate cancer and vitamin C intake; however, the findings have been inconclusive [48, 66, 124, 125]. In a case-control study conducted in Italy involving men with incident, histologically confirmed prostate cancer, there was a significant inverse association (OR 0.78, 95% CI: 0.58–0.96; P = 0.02), especially among men with the highest vitamin C intake [125]. Similar findings were reported in another case-control study where vitamin C decreased prostate cancer risks among men in the highest quartile of intake of the antioxidant (OR 0.49, 95% CI: 0.33–0.74) [66]. There are two other case control studies that have reported reduced prostate cancer risk due to vitamin C intake [48, 126]. There is also evidence in prospective studies such as the North Carolina-Louisiana Prostate Cancer Project where >1500 mg (compared with <500 mg vitamin C equivalent/day) reduced prostate cancer risk (RR 0.31, 95% CI: 0.15–0.67; P < 0.01) [127] (**Table 4**). In meta-analysis conducted by Bai and colleagues involving 103,658 subjects, dietary vitamin C intake (150 mg/

day) reduced risk among case-control studies (RR 0.79, 95% CI: 0.69–0.91, P = 0.001) and 0.95 (95% CI: 0.90–0.99, P = 0.039) in cohort studies [125].

However, a number of studies have reported no association between prostate cancer risk and vitamin C [14, 128]. In The Prostate Cancer and Environment Study (PROtEuS), a recent population-based case-control study conducted in Montreal, there was the absence of an association between overall or grade of prostate cancer incidence and either recent dietary or supplemented vitamin C uptake [129]. Key evidence also comes from the posttrial follow-up in the Physicians' Health Study II randomized trial where no effect was observed of vitamin C on incidence of prostate cancer (HR 0.99, 95% CI: 0.89–1.10) [14]. Earlier in the Physicians' Health Study II randomized controlled trial, vitamin C supplement (500 mg daily) had

hydrogen peroxide, which eventually damages the cell [123].

*DOI: http://dx.doi.org/10.5772/intechopen.85770*

nonusers [116].

damage in prostate tissue [117].

**7. Vitamin C and prostate cancer**

*Dietary Antioxidants in the Chemoprevention of Prostate Cancer DOI: http://dx.doi.org/10.5772/intechopen.85770*

*Antioxidants*

populations.

elevated risk of prostate cancer [101]. In a retrospective cohort study, higher levels of selenium were associated with decreased risk of aggressive prostate cancer (RR 0.60, 95% CI: 0.32–1.12), and the relationship at diagnosis may be modified by the manganese superoxide dismutase (SOD2) gene [105]. Furthermore, in a study involving the Within the Danish "Diet, Cancer and Health" cohort, higher levels of plasma selenium were not associated with lower risk of high-grade prostate cancer disease or prostate cancer-specific mortality [108]. A systematic review and metaanalysis of case-control studies, randomized controlled trials, and prospective cohort studies showed decreased prostate cancer risk with increasing serum/plasma selenium levels (up to 170 ng/ml) when 12 studies were analyzed and also lower risk of disease with toenail selenium levels between 0.85 and 0.94 μg/g (estimated RR 0.29, 95% CI: 0.14–0.61) in three high-quality studies [109]. Therefore, although there is evidence of a potential protective effect of selenium in terms of its status and supplementation, further studies are required especially in low-selenium status

In the last 10 years, a number of systematic and meta-analysis have been conducted to examine the relationship between selenium status and prostate cancer. In one study reported by Sayehmirj and colleagues, the relative risks for prostate cancer (based on case-control, cohort, and randomized control trials) on serum and nail samples were 0.85 (95% CI: 0.61–1.17) and 0.66 (95% CI: 0.41–1.05), respectively. They also reported a relative risk of 0.67 (95% CI: 0.52–0.87) between selenium levels and advanced prostate cancer [110]. The authors concluded that selenium supplementation could have a protective role against the initiation and progression to advanced stages [110]. A MOOSE-compliant meta-analysis of 17 studies showed a significant inverse association between prostate cancer risk and

Even though these studies suggest that higher levels of selenium are associated with decreased risk of prostate cancer; there are others that have demonstrated otherwise. An analysis of 15 prospective studies by Allen et al. failed to show any association between blood selenium levels and risk of prostate cancer (OR, 1.01, 95% CI: 0.83–1.23). However, high blood selenium levels were not associated with nonaggressive disease, but with aggressive disease (OR 0.43, 95% CI: 0.21–0.87) [111]. Another key finding in this study was that nail selenium levels were significantly inversely associated with prostate cancer risk (OR0.29, 95% CI: 0.22–0.40, P < 0.001) and also with both aggressive and nonaggressive disease [111]. Similarly, in the prospective Netherlands cohort study, toenail selenium levels were associated with a significant reduction in the risk of advanced prostate cancer (RR 0.37, 95% CI: 0.27–0.51; P < 0.001) [112]. However, in a case-control study, selenium levels in toenail were not associated with prostate cancer risk, and its supplementation while not having any effect among participants with low selenium status elevates the risk (by 91%, P = 0.07) among those with higher selenium status [42]. The authors suggest that men with low selenium status did not benefit from its supplementation which increased the risk of high-grade prostate cancer among those participants

The effects of selenium on prostate cancer remain uncertain. In a prospective cohort study in the United States, reported by Peter et al., showed that long-term selenium supplementation did not lower the overall risk of prostate cancer (HR 0.90, 95% CI: 0.62–1.3) with participants having an average intake of >50 μg/day over a 10-year period [104]. In a Cochrane review including randomized controlled trials and longitudinal observational studies, there was no association between selenium supplementation and the risk of prostate cancer [113], nor in a Mendelian randomization analysis by Yarmolinsky et al. where the authors suggested that selenium supplementation could have unfavorable effects on risks of advanced disease

serum selenium levels (RR 0.76, 95% CI: 0.64–0.76) [82].

**230**

with high selenium status [42].

[114]. There is further supporting evidence in the follow-up of the Procomb trial where there was no association between selenium supplementation and prostate cancer risk [115]. Conversely, there are studies that suggest caution with selenium supplement usage among males with prostate cancer. In the Health Professionals Follow-Up Study (over a 22-year period) of men diagnosed with nonmetastatic prostate cancer, supplementation of 140 or more μg/day of selenium had a 2.6-fold risk of prostate cancer mortality (95% CI: 1.44–4.70, P = 0.001) compared with nonusers [116].

The mechanism of action of selenium in the inhibition of cancer development could include reduction in DNA damage. Waters et al. reported that dietary supplementation of selenium increases epithelial cell apoptosis in prostate and DNA damage in prostate tissue [117].

## **7. Vitamin C and prostate cancer**

Vitamin C is mainly obtained from vegetables and fruit sources and is considered to be a very important water-soluble antioxidant [118]. Foods and supplements are sources, which provide vitamin C intake while that from foods only is referred to as dietary vitamin C. There is evidence that the mechanisms by which vitamin C prevents the harmful effects of carcinogens include decreasing oxidative DNA damage [119, 120]. Vitamin C functions as a scavenger of free radicals and, therefore, has a potential role in the chemoprevention of prostate cancer [121]. Animal and *in vitro* studies have demonstrated that it could inhibit the cell growth and viability [8]. Menon and colleagues suggested that vitamin C may be a potent anticancer agent as it inhibits tumor growth by producing reactive oxygen species [122]. In another study, vitamin C inhibits cell growth and division via the generation of hydrogen peroxide, which eventually damages the cell [123].

A number of epidemiological studies have documented the relationship between risk of prostate cancer and vitamin C intake; however, the findings have been inconclusive [48, 66, 124, 125]. In a case-control study conducted in Italy involving men with incident, histologically confirmed prostate cancer, there was a significant inverse association (OR 0.78, 95% CI: 0.58–0.96; P = 0.02), especially among men with the highest vitamin C intake [125]. Similar findings were reported in another case-control study where vitamin C decreased prostate cancer risks among men in the highest quartile of intake of the antioxidant (OR 0.49, 95% CI: 0.33–0.74) [66]. There are two other case control studies that have reported reduced prostate cancer risk due to vitamin C intake [48, 126]. There is also evidence in prospective studies such as the North Carolina-Louisiana Prostate Cancer Project where >1500 mg (compared with <500 mg vitamin C equivalent/day) reduced prostate cancer risk (RR 0.31, 95% CI: 0.15–0.67; P < 0.01) [127] (**Table 4**). In meta-analysis conducted by Bai and colleagues involving 103,658 subjects, dietary vitamin C intake (150 mg/ day) reduced risk among case-control studies (RR 0.79, 95% CI: 0.69–0.91, P = 0.001) and 0.95 (95% CI: 0.90–0.99, P = 0.039) in cohort studies [125].

However, a number of studies have reported no association between prostate cancer risk and vitamin C [14, 128]. In The Prostate Cancer and Environment Study (PROtEuS), a recent population-based case-control study conducted in Montreal, there was the absence of an association between overall or grade of prostate cancer incidence and either recent dietary or supplemented vitamin C uptake [129]. Key evidence also comes from the posttrial follow-up in the Physicians' Health Study II randomized trial where no effect was observed of vitamin C on incidence of prostate cancer (HR 0.99, 95% CI: 0.89–1.10) [14]. Earlier in the Physicians' Health Study II randomized controlled trial, vitamin C supplement (500 mg daily) had


#### **Table 4.**

*Showing studies on the effect of vitamin C on prostate cancer.*

no effect on prostate cancer (HR 1.02, 95% CI: 0.90–1.15; P = 0.80), a finding that remained even after stratification by various cancer risk factors [128]. Further, a systematic review of nine randomized controlled trials found no significant effects of vitamin C supplementation (RR 0.98, 95% CI: 0.91–1.06) on prostate cancer incidence [130] (**Table 4**).

Studies involving the use of supplements might favor results that are bias as the period of use may be relatively short term, associated health problems in persons who use vitamin C supplements, and the different biological activity or absorption contributing to the possibly different effects of dietary compared with supplemental use of vitamin C [121, 131].

The studies cited above on vitamin C and prostate cancer risk provide inconclusive evidence. While some case-control studies demonstrate a protective effect, randomized trials and meta-analysis fail to clearly demonstrate any beneficial effect of vitamin C on the risk of prostate cancer.

### **8. Conclusion**

The effect of dietary and supplemental antioxidants on risk of prostate cancer remains undecided and inconclusive. More epidemiological and human clinical trials as well as animal studies are needed to give an improved understanding on the biology of prostate cancer and how antioxidants at supranutritional and nutritional levels influence the risk of prostate cancer.

#### **Nothing to disclose**

The authors have no funding and conflicts of interest to disclose regarding the content of this chapter.

**233**

**Author details**

Dwayne Tucker1

Lennox Anderson-Jackson1

provided the original work is properly cited.

, Melisa Anderson1

University College, Kingston, Jamaica, West Indies

\*Address all correspondence to: dmcgrowd@yahoo.com;

West Indies, Kingston, Jamaica, West Indies

West Indies, Kingston, Jamaica, West Indies

donovan.mcgrowder@uwimona.edu.jm

*Dietary Antioxidants in the Chemoprevention of Prostate Cancer*

*DOI: http://dx.doi.org/10.5772/intechopen.85770*

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

, Fabian Miller2,3, Kurt Vaz1

\*

and Donovan McGrowder1

2 Department of Physical Education, Faculty of Science and Technology, The Mico

3 Biotechnology Centre, Faculty of Science and Technology, The University of the

1 Department of Pathology, Faculty of Medical Sciences, The University of the

,

*Dietary Antioxidants in the Chemoprevention of Prostate Cancer DOI: http://dx.doi.org/10.5772/intechopen.85770*
