The SULT1 family, which comprises at least 11 isoforms, is highly expressed in the liver, but is also present in other extrahepatic tissues.130 SULT1A1 is mainly a liver form of the enzyme but is also detectable in the brain, breast, intestine, endometrium, kidney, lung, and platelets. Transcripts for the SULT1B subfamily, which is mainly involved in the sulfation of thyroid hormones, have been detected in the liver, colon, small intestine, and blood leukocytes, whereas human SULT1C2 transcript is detected primarily in the thyroid, stomach, and kidney. SULT1C4 transcripts are found predominantly in fetal kidney and lung and have been detected in the adult brain and ovary. Human SULT1E1 and 1E2 are found in steroid hormone-responsive tissues including the endometrium, testis, breast, adrenal gland, and placenta, in addition to the liver and intestine. The SULT2 family, including transcripts for SULT2A1 and SULT2A2, have been found in adrenal cortex, liver, brain, and intestine.
The ontogeny of SULTs was studied recently by Richard et al}xz in the developing liver, lung, and brain. SULT1A1 enzymatic activity was higher in fetal tissues than in postnatal liver. Also SULT1A3 was expressed at higher levels in early stages of development, decreased gradually in the late fetal/early neonatal liver and was not observed in adult liver. In the lung, high SULT1A3 activity was observed in the fetus compared to neonatal levels. Therefore, the developing fetus clearly possesses significant sulfation capabilities. This could be a consequence of the important role sulfation plays in the homeostasis of hormones and other endogenous compounds that are important for development or because of the need for xenobiotic detoxification in the fetus where other conjugating enzymes, notably the UGTs, are not expressed at high levels until the neonatal stage.
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