An occurrence study was conducted to measure five iodo-acids (iodoacetic acid, bromoiodoacetic acid, (Z)-3-bromo-3-iodo-propenoic acid, (E)-3-bromo-3-iodo-propenoic acid, and (E)-2-iodo-3-methylbutenedioic acid) and two iodo-trihalomethanes (iodo-THMs), (dichloroiodomethane and bromochloroiodomethane) in chloraminated and chlorinated drinking waters from 23 cities in the United States and Canada. Since iodoacetic acid was previouslyfound to be genotoxic in mammalian cells, the iodo-acids and iodo-THMs were analyzed for toxicity. A gas chromatography (GC)/negative chemical ionization-mass spectrometry (MS) method was developed to measure the iodo-acids; iodo-THMs were measured using GC/high resolution electron ionization-MS with isotope dilution. The iodo-acids and iodo-THMs were found in waters from most plants, at maximum levels of 1.7 microg/L (iodoacetic acid), 1.4 microg/L (bromoiodoacetic acid), 0.50 microg/L ((Z)-3-bromo-3-iodopropenoic acid), 0.28 microg/L ((E)-3-bromo-3-iodopropenoic acid), 0.58 microg/L ((E)-2-iodo-3-methylbutenedioic acid), 10.2 microg/L (bromochloroiodomethane), and 7.9 microg/L (dichloroiodomethane). Iodo-acids and iodo-THMs were highest at plants with short free chlorine contact times (< 1 min), and were lowest at a chlorine-only plant or at plants with long free chlorine contact times (> 45 min). Iodide levels in source waters ranged from 0.4 to 104.2 microg/L (when detected), but there was not a consistent correlation between bromide and iodide. The rank order for mammalian cell chronic cytotoxicity of the compounds measured in this study, plus other iodinated compounds, was iodoacetic acid > (E)-3-bromo-2-iodopropenoic acid > iodoform > (E)-3-bromo-3-iodo-propenoic acid > (Z)-3-bromo-3-iodo-propenoic acid > diiodoacetic acid > bromoiodoacetic acid > (E)-2-iodo-3-methylbutenedioic acid > bromodiiodomethane > dibromoiodomethane > bromochloroiodomethane approximately chlorodiiodomethane > dichloroiodomethane. With the exception of iodoform, the iodo-THMs were much less cytotoxic than the iodo-acids. Of the 13 compounds analyzed, 7 were genotoxic; their rank order was iodoacetic acid >> diiodoacetic acid > chlorodiiodomethane > bromoiodoacetic acid > E-2-iodo-3-methylbutenedioic acid > (E)-3-bromo-3-iodo-propenoic acid > (E)-3-bromo-2-iodopropenoic acid. In general, compounds that contain an iodo-group have enhanced mammalian cell cytotoxicity and genotoxicity as compared to their brominated and chlorinated analogues.

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The stereochemistry of several sterol precursors and end products synthesized by two fungal-like microorganisms Prototheca wickerhamii (I) and Dictyostelium discoideum (H) have been determined by chromatographic (TLC, GLC, and HPLC) and spectral (UV, MS,-and 'H NMR) methods. From I and H the following sterols were isolated from the cells : cycloartenol, cyclolaudenol, 24(28)-methylenecycloartanol, ergosterol, protothecasterol, 4a-methylergostanol, 4a-methylclionastanol, clionastanol, 2413-ethylcholesta-8,22-enol, and dictyosterol. In addition, the mechanism of C-24 methylation was investigated in both organisms by feeding to I[2-3H]lanosterol, [2-3H] Based on what is known in the literature regarding sterol distribution and phylogenesis together with our rmdings that the stereochemical outcome of squalene oxide cyclization leads to the production of cycloartenol rather than lanosterol (characteristic of the fungal genealogy) and the chirality of the C-24 alkyl group is similar in the two nonphotosynthetic microbes (Ji oriented), we conclude that Prototheca is an apoplastic Chlorelia (i.e., an alga) and that Dictyostelium as well as the other soil amoebae that synthesize cycloartenol evolved from algal rather than fungal ancestors.The sterol pathway is thought to be very ancient, perhaps having arisen during the later stages of prokaryote evolution (1, 2). True sterols-e.g., end products such as cholesterolare antedated by the production of sterol-like compoundse.g., pentacyclic triterpenoids (3-6)-which were formed in the Precambrian anaerobic environment by the cyclization of squalene. Once molecular oxygen was in sufficient quantity in the atmosphere to permit squalene oxide genesis, a switching mechanism became operative to divert squalene from pentacyclic triterpenoid production to sterol synthesis (6, 7). The first compounds derived by the anaerobic cyclization of squalene oxide are the tetracyclic stereoisomers cycloartenol and lanosterol. Neither stereoisomer is known to be formed by cyclization in the same organism, whether the latter is a prokaryote or a eukaryote (2). This bifurcation in the sterol pathway is now recognized in biochemical textbooks (8-10) and in reviews on evolution (11-13) as a means to dissociate groups of organisms with an evolutionary history of oxygenic photosynthesis-e.g., as detected through the stereospecific formation of cycloartenol and its further metabolism of the 96,19-cyclopropyl ring-from those nonphotosynthetic progenitors and their descendants, which possess a lanosterolbased pathway (2). The association of the cycloartenol route and the endosymbiotic origin and subsequent loss of the chloroplast in some nonphotosynthetic systems is not clear. The biosynthesis of cycloartenol occurs in microsomes (14) and proceeds when the chloroplast is absent (15-18). In neither case is the biosynthesis of the stereoisomer influenced by the structure of the functional steroid at the end of the pathway, and their occurrence is not influenced by the molecular clock or mutatio...