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Gene & Protein in Disease Natural carotenoids prevent prostate cancer
on PCa, increasing the risk by 42%. Asian individuals crucial to understand the correlation between ultraviolet
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exhibit a polymorphism of the xeroderma pigmentosum radiation exposure and vitamin D levels in combination
complementary group C (XPC) gene, which is associated with the risk of PCa. 43,48
with nucleotide excision repair against DNA damage. Exposure to heavy metals in the environment, such
Studies on the XPC gene have demonstrated that intron as cadmium, zinc, lead, and arsenic, may be correlated
9 (PAT) polymorphism is associated with a higher risk with the risk of PCa. Cadmium pollutes the environment
of PCa. Asian smokers with one or two alleles of PAT through industrial and agricultural activities. Workers with
polymorphism have a higher incidence of this cancer. prolonged exposure (exceeding 5 years) to cadmium have
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Smoking can also increase the risk of mortality in PCa. demonstrated an increased incidence of PCa compared
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On the other hand, Pourmand et al. have demonstrated in to other populations. While mortality rates were high
their study that smoking does not affect the risk of PCa in several studies, this correlation was not universally
in Iranian people. Male smokers exhibit increased levels observed. 49-52 Environmental exposure to zinc has not been
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of androgens, which may contribute to PCa risk. The extensively analyzed. Zinc is commonly found in water
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mechanism of smoking interaction in PCa progression is and soil. Wagner et al. reported that low levels of zinc
still controversial and requires further study. 27 concentration in the soil of certain areas of South Carolina
Alcohol consumption has been associated with an were correlated with a high incidence of PCa in the male
increased risk of various cancers in humans. Bergengren population. 52,53 Zinc levels were found to be 60 – 70% lower
et al. briefly described the lack of correlation between in PCa patients than in normal individuals. Lead workers
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alcohol consumption and the risk of PCa. However, may also be at risk for PCa. Siddiqui et al. found higher lead
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contrasting findings from other studies have demonstrated concentrations in PCa patients. Arsenic has been found
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that alcohol consumption does pose a moderate, yet in groundwaters. High levels of arsenic exposure through
statistically significant, risk for PCa, particularly in drinking water have been associated with an increased risk
relation to alcohol dose. A review conducted by Perdana of PCa. 52
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et al. indicates a dose-risk relationship, suggesting that Synthetic hormones, such as bisphenol A (BPA), can
consuming four drinks per day is associated with a higher contribute to the risk of prostate carcinogenesis. BPA, a
risk of PCa, but moderate intake of red wine may have a synthetic estrogen, is found in food and dental supplies.
protective impact. 16,21 Several factors contribute to the Exposure to BPA can occur through air, oral ingestion, or skin
varying results regarding alcohol as a risk factor, such as contact, potentially increasing the risk of PCa development. 10
the different types of alcohol consumed, dietary habits, and
alcohol consumption history. Men with a long history of 1.4. Link between carotenoids and cancer
alcohol consumption over many years have a high incidence The evidence suggests a protective role of carotenoids
of developing PCa. In addition, men with a family history in commonly diagnosed cancers, with breast cancer
of PCa may need to exercise caution with alcohol use. 42
comprising the most frequent type among women. A
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1.3.9. Environmental agents meta-analysis of 33 observational studies revealed that
dietary α-carotene was associated with a 9% (relative risk
Except for nutritional and genetic risk factors, environmental [RR] = 0.91, 95% confidence interval [CI] = 0.85 – 0.98) and
agents must be considered in the risk factors for PCa. 18% (odds ratio [OR] = 0.82, 95% CI = 0.70 – 0.97) decreased
Studies have associated sunlight, trace minerals, farming, risk for breast cancer when comparing the highest with the
and synthetic hormones as potential risk factors for PCa. lowest intakes, according to pooled data from cohort and
Farmers, in particular, exhibit a higher risk of incidence case–control studies, respectively. Similar results were
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and mortality than other workers, possibly attributed observed for β-carotene, with the respective decrease in
to pesticide exposure, such as phorate, coumaphos, and the risk being 6% (RR = 0.94, 95% CI = 0.88 – 1.00) and
butylate. 10,43 Butylate, coumaphos, and phorate have been 25% (OR = 0.75, 95% CI = 0.67 – 0.85). A dose-response
associated with a high incidence of PCa, especially in men relationship between higher carotenoid consumption
with a family history of this cancer, but not among men and decreased risk was revealed only for β-carotene. In
without a family history. 44-46 Koutros et al. linked the risk of addition, a pooled analysis of eight prospective studies
PCa among farmers to pesticide exposure, potentially due involving 3,055 cases and 3,956 controls indicated a
to a mutation in chromosome 8q24. 47 reduced risk of breast cancer in those in the top quantile of
Low exposure to sunlight (ultraviolet radiation) plasma total carotenoids (RR = 0.81, 95% CI = 0.68 – 0.96),
and low levels of vitamin D may interact with prostate β-carotene (RR = 0.83, 95% CI = 0.70 – 0.98), and lycopene
carcinogenesis in young men. Further investigation is (RR = 0.78, 95% CI = 0.62 – 0.99) compared to those in the
Volume 3 Issue 1 (2024) 5 https://doi.org/10.36922/gpd.2827

