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[
Lipids,
1987]
The metabolism of three dietary 4,4-desmethylsterols and two 4 alpha- methylsterols was investigated in the free-living nematode Caenorhabditis elegans. Dietary cholestanol was converted mostly to lathosterol. Dietary lathosterol, 7-dehydrocholesterol, 4 alpha- methylcholest-7-enol and 4 alpha-methylcholest-8(14)-enol each remained largely unchanged. An absolute requirement for a substantial quantity of 7-dehydrocholesterol in C. elegans did not exist. C. elegans was unable to remove a 4 alpha-methyl group or introduce a double bond at C-5 and also demonstrated the lack of a delta 7- reductase. Its nutritional sterol requirement was satisfied by cholestanol, lathosterol or 7-dehydrocholesterol; growth was comparable to that obtained previously in media containing delta 5- sterols. However, the two 4 alpha-methylsterols appeared to be unsatisfactory sterol nutrients. The possible physiological importance of 4 alpha-methylsterols is discussed briefly.
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[
Lipids,
1985]
The metabolism of 4 dietary 24-alkylsterols was investigated in the free-living nematode Caenorhabditis elegans. The major unesterified sterols of C. elegans in media supplemented with either campesterol, 22-dihydrobrassicasterol or stigmasterol included cholesta-5,7-dienol, cholesterol, cholest-7-enol, and 4a-methylcholest-8(14)-enol. Dietary stigmastanol yielded cholest-7-enol, cholestanol, cholest-8(14)-enol, and 4a-methylcholest-8(14)-enol as major unesterified sterols. Esterified sterols comprised less than 22% of the total sterol. Removal of a C-24 ethyl substituent of sterols was neither hindered by the presence of a delta22-bond in the sterol side chain nor was it dependent on unsaturation in ring B of the steroid nucleus. C. elegans reduced a delta22-bond during its metabolism of stigmasterol; it did not introduce a delta5-bond during stigmastanol metabolism. C. elegans was capable of removing a C-24 methyl substituent regardless of it stereochemical orientation. Metabolic processes involving the steroid ring system of cholesterol (C-7 dehydrogenation, delta5-reduction, 4a-methylation, delta8(14)-isomerization) in C. elegans were not hindered by the presence of a 24-methyl group; various 24-methylsterol metabolites from campesterol were detected, mostly 24-methylcholesta-5,7-dienol. In contrast, no 24-ethylsterol metabolites from the dietary ethylsterols were found. More dietary 24-methylsterol remained unmetabolized than did dietary 24-ethylsterol. A 24a-ethyl group and a 24B-methyl group were dealkylated to a greater extent by C. elegans than was a 24a-methyl group, perhaps reflecting the substrate specificity of the dealkylation enzyme system, or suggesting different enzymes
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[
Lipids,
1985]
Effects on the metabolism of campesterol and stigmasterol in Caenorhabditis elegans were investigated using N,N- dimethyldodecanamine, a known inhibitor of growth, reproduction and the delta 24-sterol reductase of this nematode. 7-Dehydrocholesterol was the predominant sterol (51%) of C. elegans grown in stigmasterol- supplemented media, whereas addition of 25 ppm amine resulted in a large decrease in the relative percentage of 7-dehydrocholesterol (23%) and the accumulation of a substantial proportion (33%) of delta 24-sterols (e.g., cholesta-5,7,24-trienol) and delta 22,24-sterols (e.g., cholesta-5,7,22, 24-tetraenol) but yielded no delta 22- sterols. Dealkylation of stigmasterol by C. elegans proceeded in the presence of the delta 22-bond; reduction of the delta 22-bond occurred prior to delta 24-reduction. Addition of 25 ppm amine to campesterol-supplemented media altered the sterol composition of C. elegans by increasing the percentage of unmetabolized dietary campesterol from 39 to 60%, decreasing the percentage of 7- dehydrocholesterol from 26 to 12%, and causing the accumulation of several delta 24-sterols (6%). C. elegans also was shown to be capable of dealkylating a delta 24 (28)-sterol as it converted 24- methylenecholesterol to mostly 7-dehydrocholesterol. The proposed role of 24-methylenecholesterol as an intermediate between campesterol and 7-dehydrocholesterol was supported by the
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[
Comp Biochem Physiol C,
1984]
An analogous series of dimethylalkyl compounds, consisting of four amines, an amide, and a phosphonate ester, inhibited motility and reproduction of the nematode Caenorhabditis elegans. Dimethylamines with straight-chain lengths of 12, 14, or 16 carbon atoms were equally active nematicides, causing greater than 80% population growth inhibition at a concentration of 25 ppm. The C12 straight- chain amine and its corresponding amide produced similar inhibition and were much more potent than either the corresponding C12 phosphonate or a C12 branched-chain amine. Inhibition of the delta 24- sterol reductase system was exhibited by all four amines, but not by the amide or phosphonate, in the following order of activity: C12 branched-chain amine greater than C12 straight-chain amine greater than C14 amine greater than C16 amine. The C12 branched amine also blocked the C-24(28)-dehydrogenase system in the conversion of sitosterol to fucosterol, the initial step in sitosterol dealkylation.
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[
J Nematol,
1986]
Current knowledge of steroid nutrition, metabolism, and function in free-living, plant-parasitic and animal-parasitic nematodes is reviewed, with emphasis upon recent investigation of Caenorhabditis elegans. A number of 4-desmethylsterols with a trans-A/B ring configuration can satisfy the steroid nutritional requirement in C. elegans, but sterols with a cis-A/B ring configuration or trans-A/B sterols with a 4-methyl group cannot. C. elegans removes methyl or ethyl substituents at C-24 of the plant sterols sitosterol, campesterol, stigmasterol, stigmastanol, and 24-methylene-cholesterol to produce various sterols with structures partially dependent upon that of the dietary sterol. Additional metabolic steps in C. elegans include reduction of Delta(2)(2)- and Delta-bonds, C-7 dehydrogenation, isomerization of a Delta-bond to a Delta(1)-bond, and 4alpha-methylation. An azasteroid and several long-chain alkyl amines interfere with the dealkylation pathway in C. elegans by inhibiting the Delta(2)-sterol reductase; these compounds also inhibit growth and reproduction in various plant-parasitic and animal-parasitic nematodes. A possible hormonal role for various steroids identified in nematodes is discussed.
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[
Zootaxa,
2022]
Rhagovelia medinae sp. nov., of the hambletoni group (angustipes complex), and R. utria sp. nov., of the hirtipes group (robusta complex), are described, illustrated, and compared with similar congeners. Based on the examination of type specimens, six new synonymies are proposed: R. elegans Uhler, 1894 = R. pediformis Padilla-Gil, 2010, syn. nov.; R. cauca Polhemus, 1997 = R. azulita Padilla-Gil, 2009, syn. nov., R. huila Padilla-Gil, 2009, syn. nov., R. oporapa Padilla-Gil, 2009, syn. nov, R. quilichaensis Padilla-Gil, 2011, syn. nov.; and R. gaigei, Drake Hussey, 1947 = R. victoria Padilla-Gil, 2012 syn. nov. The first record from Colombia is presented for R. trailii (White, 1879), and the distributions of the following species are extended in the country: R. cali Polhemus, 1997, R. castanea Gould, 1931, R. cauca Polhemus, 1997, R. gaigei Drake Hussey, 1957, R. elegans Uhler, 1894, R. femoralis Champion, 1898, R. malkini Polhemus, 1997, R. perija Polhemus, 1997, R. sinuata Gould, 1931, R. venezuelana Polhemus, 1997, R. williamsi Gould, 1931, and R. zeteki Drake, 1953.
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[
Lipids,
1984]
The metabolism of various dietary sterols and the effects of an azasteroid on sitosterol metabolism in the free-living nematode Caenorhabditis elegans was investigated. The major unesterified sterols of C. elegans in media supplemented with sitosterol, cholesterol or desmosterol included 7-dehydrocholesterol (66.5%, 40.5%, 31.2%, respectively), cholesterol (6.7%, 52.3%, 26.9%), lathosterol (4.4%, 3.6%, 1.7%) and 4a-methylcholest-8(14)-en-3B-ol (4.2%, 2.1%, 3.8%). Esterified sterols, representing less than 20% of the total sterols, were somewhat similar except for a significantly higher relative content of 4a-methylcholest-8(14)-en-3B-ol (23.3%, 23.4%, 10.6%). Thus C. elegans not only removes the substituent at C24 of dietary sitosterol but possesses the unusual ability to produce significant quantities of 4a-methylsterols. When C. elegans was propagated in medium supplemented with sitosterol plus 5 ug/ml of 25-azacoprostane hydrochloride, the azasteroid stronly interfered with reproduction and motility of C. elegans and strongly inhibited the delta24-sterol reductase enzyme system; excluding sitosterol, the major free sterols of azacoprostane-treated C. elegans were cholesta-5,7,24-trien-3B-ol (47.9%), desmosterol (9.4%), fucosterol (2.1%) and cholesta-7,24-
dien-3B-ol (2.0%). These 4 sterols are likely intermediates in the metabolism of sitosterol in C. elegans.
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[
Trop Med Int Health,
1999]
OBJECTIVE AND METHOD: To compare the utility of an ELISA using 3 recombinant antigens with that of the skin biopsy to estimate incidence of infections in a sentinel cohort of individuals living in an endemic community in southern Mexico during a set of 11 subsequent ivermectin treatments. RESULTS: The apparent community prevalence of infection and microfilarial skin infection before and after 11 treatments with ivermectin plus nodulectomy were 78% and 13%, and 0.68 mf/mg and 0.04 mf/mg, respectively, as measured by skin biopsy. Of a group of 286 individuals participating in all surveys, a sentinel cohort of 42 mf and serologically negative individuals had been followed since 1994. The annual percentage of individuals becoming positive in this cohort was 24% (10/42), 28% (9/33), 0%, and 4.3% (1/23) in 1995, 1996, 1997 and 1998, respectively. Likewise, the incidence in children 5 years and under (n = 13) within this sentinel cohort was 15% (2/13), 18% (2/11), 0% and 11% (1/9), respectively. All individuals became positive to both tests simultaneously, indicating that seroconversion assessed infection incidence as accurately as skin biopsy in the sentinel group. CONCLUSION: Incidence monitoring of a sentinel cohort provides an estimation of the parasite transmission in the community; it is less costly than massive sampling, and a finger prick blood test might be more acceptable in some communities.
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[
Steroids,
1986]
Panagrellus redivivus produced 24-methyl-23-dehydrocholesterol as 4.0% of the 4-desmethylsterols when propagated in a medium containing campesterol as the dietary sterol. The re-examination of previous data revealed that Caenorhabditis elegans produced 1.8% 24-methyl-23-dehydrocholesterol when propagated in medium containing campesterol. 24-Methyl-23-dehydrocholesterol was not detected when the nematodes were propagated in medium containing 22-dihydrobrassicasterol or 24-methylenecholesterol. This may be a result of the greater efficiency of dealkylation of the latter two sterols. This is the first report of the natural occurrence of this sterol in a non-photosynthetic organism, and the first report in organisms that dealkylate 24-alkylsterols.
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[
Steroids,
1983]
Caenorhabditis elegans possesses a unique sterol methylation pathway not reported to occur in any other organism and also removes the C-24 ethyl group of sitosterol (a plant sterol). This nematode produced substantial quantities of 4 alpha-methyl-5 alpha-cholest-8(14)-en-3 beta-ol and smaller amounts of lophenol from dietary cholesterol, desmosterol or sitosterol. When C. elegans was propagated in media containing sitosterol plus 25-azacoprostane hydrochloride (25-
aza-5 beta-cholestane hydrochloride), an inhibitor of delta 24-sterol reductase in insects, its 4 alpha-methylsterol fraction largely consisted of equal amounts of 4 alpha-methyl-5 alpha-cholesta-7,24-
dien-3 beta-ol and 4 alpha-methyl-5 alpha-cholesta-8(14),24-
dien-3 beta-ol. Thus 25-azacoprostane hydrochloride inhibited both a delta 24-sterol reductase and a delta 7-sterol isomerase