J
James Michael H
Guest
Flavonoids and Protection from Cancer: Enhancement of DHEA?
Copyright 2004, James Michael Howard, Fayetteville, Arkansas, U.S.A.
It is my hypothesis that low dehydroepiandrosterone (DHEA) may trigger cancer. Therefore, when the
background source of DHEA in the blood, DHEAsulfate, is high at the expense of being desulfonated
into the active form, DHEA, the incidence of cancer may increase. It is known that "flavonoids"
protect against cancer. I suggest this is the result of flavonoids inhibiting the formation of
DHEAsulfate from DHEA. In other words, flavonoids may protect against cancer by helping to maintain
the levels of DHEA, that is, flavonoids help maintain a higher DHEA to DHEAsulfate ratio. (Please
read the abstract below.) I invite you to read my explanation of the connection of DHEA with cancer
at www.anthropogeny.com/research.html ; look for "How 'Hormone Replacement Therapy' (HRT) May Cause
Breast Cancer."
"Inhibition of rat liver sulfotransferases SULT1A1 and SULT2A1 and glucuronosyltransferase by
dietary flavonoids."
Mesia-Vela S, Kauffman FC.
"1. Dietary flavonoids including kaempferol, quercetin, genistein and daidzein were tested for their
ability to alter the conjugation of oestradiol (E(2)) via rat liver sulfotransferases and
glucuronosyltransferase. 2. All four flavonoids inhibited the sulfonation of E(2) via phenol
sulfotransferase, SULT1A1 with
IC(50)s ranging from 0.29 to 4.61 micro M. Sulfonation of dehydroisoandrosterone (DHEA) via
hydroxysteroid sulfotransferase, SULT2A1, was inhibited by higher amounts of the flavonoids
(IC(50)s ranging from 34 to 116 micro M). 3. All flavonoids inhibited the formation of E(2)-beta-
glucuronides (at carbon atoms 3 and 17) with IC(50)s ranging from 43 to 260 micro M.
Glucuronidation of 4-methylumbelliferone (4-MU) was inhibited by high amounts of the
flavonoids
(IC(51)s ranging from 860 to 1550 micro M). 4. Hydrolysis of sulfonated oestrogens via arylsulfatase-
c (ARSC) or 4-methylumbelliferone beta-glucuronidate (MUG) were not inhibited by the
flavonoids. 5. It is concluded that SULT1A1 but not SULT2A1 or glucuronosyltransferase is
highly sensitive to inhibition by dietary flavonoids. The potency of the inhibition for
SULT1A1 (quercetin > kaempferol > genistein > daidzein) suggests a dependency on the number
and position of hydroxyl radicals in the flavonoid molecule." Xenobiotica. 2003 Dec;
33(12): 1211-20.
Copyright 2004, James Michael Howard, Fayetteville, Arkansas, U.S.A.
It is my hypothesis that low dehydroepiandrosterone (DHEA) may trigger cancer. Therefore, when the
background source of DHEA in the blood, DHEAsulfate, is high at the expense of being desulfonated
into the active form, DHEA, the incidence of cancer may increase. It is known that "flavonoids"
protect against cancer. I suggest this is the result of flavonoids inhibiting the formation of
DHEAsulfate from DHEA. In other words, flavonoids may protect against cancer by helping to maintain
the levels of DHEA, that is, flavonoids help maintain a higher DHEA to DHEAsulfate ratio. (Please
read the abstract below.) I invite you to read my explanation of the connection of DHEA with cancer
at www.anthropogeny.com/research.html ; look for "How 'Hormone Replacement Therapy' (HRT) May Cause
Breast Cancer."
"Inhibition of rat liver sulfotransferases SULT1A1 and SULT2A1 and glucuronosyltransferase by
dietary flavonoids."
Mesia-Vela S, Kauffman FC.
"1. Dietary flavonoids including kaempferol, quercetin, genistein and daidzein were tested for their
ability to alter the conjugation of oestradiol (E(2)) via rat liver sulfotransferases and
glucuronosyltransferase. 2. All four flavonoids inhibited the sulfonation of E(2) via phenol
sulfotransferase, SULT1A1 with
IC(50)s ranging from 0.29 to 4.61 micro M. Sulfonation of dehydroisoandrosterone (DHEA) via
hydroxysteroid sulfotransferase, SULT2A1, was inhibited by higher amounts of the flavonoids
(IC(50)s ranging from 34 to 116 micro M). 3. All flavonoids inhibited the formation of E(2)-beta-
glucuronides (at carbon atoms 3 and 17) with IC(50)s ranging from 43 to 260 micro M.
Glucuronidation of 4-methylumbelliferone (4-MU) was inhibited by high amounts of the
flavonoids
(IC(51)s ranging from 860 to 1550 micro M). 4. Hydrolysis of sulfonated oestrogens via arylsulfatase-
c (ARSC) or 4-methylumbelliferone beta-glucuronidate (MUG) were not inhibited by the
flavonoids. 5. It is concluded that SULT1A1 but not SULT2A1 or glucuronosyltransferase is
highly sensitive to inhibition by dietary flavonoids. The potency of the inhibition for
SULT1A1 (quercetin > kaempferol > genistein > daidzein) suggests a dependency on the number
and position of hydroxyl radicals in the flavonoid molecule." Xenobiotica. 2003 Dec;
33(12): 1211-20.