Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony.

Abstract

Unlike inorganic arsenic, inorganic trivalent antimony (Sb) is not methylated in vivo. It is excreted in the bile after conjugation with glutathione and also in urine. A significant proportion of that excreted in bile undergoes an enterohepatic circulation. In workers exposed to pentavalent Sb, the urinary Sb excretion is related to the intensity ofexposure. It has been estimated that after eight hours exposure to 500 ug SbIm', the increase of urinary Sb concentration at the end of the shift amounts on average to 35 pg/g creatinine. Antimony (Sb) and its compounds are mainly used for the production of alloys, flame retardants, and in the glass industry. Some derivatives are also used in the treatment of tropical diseases. Antimony resembles arsenic in its chemical properties; both belong to the same group (Va) of the periodic table. Knowledge of the metabolism of inorganic Sb in mammals, however, is more limited than that of arsenic.'2 Studies in animals have suggested that trivalent Sb is excreted mainly in the faeces and to a lesser extent in urine whereas the reverse holds true for pentavalent Sb. Increased urinary excretion of Sb has been found in workers exposed to Sb,03 in a glass producing factory.3This paper summarises the results of experimental studies designed to assess the handling of inorganic trivalent Sb in vivo, in particular to determine

Estimating perchlorate exposure from food and tap water based on US biomonitoring and occurrence data

“…Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al, 1998). Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999NHANES -2000NHANES , 2001NHANES -2002NHANES , and 2003NHANES -2004, even when exposure levels were below workplace air standards (Bailly et al, 1991;Iavicoli et al, 2002;Kentner et al, 1995;Liao Y-H et al, 2004;Ludersdorf et al, 1987).…”

Transition metal ions and selenite modulate the methylation of arsenite by the recombinant human arsenic (+3 oxidation state) methyltransferase (hAS3MT)

“…It is generally accepted that inorganic arsenicals are methylated by arsenic(+3) methyltransferase (AS3MT) through repetitive reduction and oxidative methylation to form pentavalent methylated arsenicals, such as monomethylarsonic acid (MMA V ) and dimethylarsinic acid (DMA V ), which are excreted mainly in urine [46][47][48]. Various reports have implicated different steps in this pathway as being susceptible to inhibition by selenite, antimonite, and other substances [14,15,[26][27][28][29][30][31][32][33]. However, there are no data about the influence of metal ions on the iAs 3+ methylation by purified enzyme at the present time and neither the inhibition mechanisms.…”

“…In addition, the combined effects of arsenic and antimony compounds have been studied in mammalian systems. IAs 3+ methylation, in rat liver cytosol, is completely inhibited by SbCl 3 [26], and the chromosome mutagenicity induced by iAs is significantly suppressed by antimony(+3) in the micronucleus test with V79 cells [27]. The iAs 3+ methylation is dramatically inhibited by antimony(+3) while the methylation of antimony is accelerated in the presence of iAs 3+ by Scopulariopsis brevicaulis [28].…”

Biotransformation of metal(loid)s by intestinal microorganisms

“…In experiments with bile duct-cannulated male Wistar rats, significant enterohepatic circulation for Sb, but no methylated Sb species were observed in bile or urine samples [103]. In contrast, both in pure culture experiments with intestinal micro organisms [85] as well as incubation experiments with fresh fecal slurries [86] or microbiocenosis from the SHIME system [87], trimethylstibine [(CH 3 ) 3 Sb, TMSb] has been detected, which has been reported to be genotoxic [104].…”