Hot water extracts from broccoli sprouts trigger induction of carcinogen-detoxification enzymes in prostate tissues.

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Intake of vegetables, particularly cruciferous vegetables, reduces prostate cancer risks.¹ Sulforaphane, an isothiocyanate present in cruciferous vegetables, may protect against cancer development by inducing the expression of carcinogen-detoxification enzymes, such as glutathione S- transferases (GSTs).^2,3 Upon consumption of glucosinolate compounds in cruciferous vegetables, isothiocyanates can be released during chewing via exposure of the glucosinolates to the plant enzyme myrosinase (thioglucoside glucohydrolase). In order to test whether sulforaphane and other isothiocyanates in broccoli sprouts can elevate the expression of chemoprotective enzymes in prostate tissues, both purified sulforaphane and a hot water extract of broccoli sprouts (broccoli sprout tea) were administered to adult male Fisher 344 rats, prone to develop prostate cancer when exposed to heterocyclic amine carcinogens,⁴ by gastric gavage. To monitor carcinogen-detoxification enzyme expression, RNA- and protein-containing extracts were prepared from liver, intestine, spleen and prostate tissues recovered 48 hours after treatment. GST activity was assessed using a CDNB assay.⁵ The expression of mRNAs encoding other chemoprotective enzymes was evaluated via hybridization to Affymetrix expression arrays. The results were that while both sulforaphane and broccoli sprout tea triggered increases in GST activity in the liver and the intestine, in a dose dependent manor, only the broccoli sprout tea caused increased GST activity in the prostate. mRNA expression profiling confirmed an induction of transcripts encoding chemoprotective enzymes in the different tissues. These findings suggest that consumption of cruciferous vegetables, containing glucosinolates, may effectively augment carcinogen defenses both in major metabolic organs, such as the liver and the intestine, as well as in cancer-prone organs, such as the prostate. References: ¹Cohen JH et al. J. Natl. Cancer Inst. 92:61-68 (2000). ²Fahey JW et al. Proc. Natl. Acad. Sci., 94:10367-10372 (1997). ³Talalay P et al. Adv Enzyme Regul., 43:121-134 (2003). Shirai T et al. Cancer Res. 57:195-198 (1997). ⁵Habig WH et al. J. Biol. Chem. 249:7130-7139 (1974).