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PubMed2025

Functional Characterization of Luciferase in a Brittle Star Indicates Parallel Evolution Influenced by Genomic Availability of Haloalkane Dehalogenase.

Determining why convergent traits use distinct versus shared genetic components is crucial for understanding how evolutionary processes generate and sustain biodiversity. However, the factors dictating the genetic underpinnings of convergent traits remain incompletely understood. Here, we use heterologous protein expression, biochemical assays, and phylogenetic analyses to confirm the origin of a luciferase gene from haloalkane dehalogenases in the brittle star Amphiura filiformis. Through database searches and gene tree analyses, we also show a complex pattern of the presence and absence of haloalkane dehalogenases across organismal genomes. These results first confirm parallel evolution across a vast phylogenetic distance, because octocorals like Renilla also use luciferase derived from haloalkane dehalogenases. This parallel evolution is surprising, even though previously hypothesized, because many organisms that also use coelenterazine as the bioluminescence substrate evolved completely distinct luciferases. The inability to detect haloalkane dehalogenases in the genomes of several bioluminescent groups suggests that the distribution of this gene family influences its recruitment as a luciferase. Together, our findings highlight how biochemical function and genomic availability help determine whether distinct or shared genetic components are used during the convergent evolution of traits like bioluminescence.

Echinodermata↗
PubMed2025

Glioma mutational signatures associated with haloalkane exposure are enriched in firefighters.

BACKGROUND: Glioma is the most common malignant primary brain tumor and is associated with significant morbidity and mortality. Modifiable risk factors remain unidentified. New advances in exposure assessment, genomic analyses, and statistical techniques permit more accurate evaluation of glioma risk associated with exogenous occupational or environmental exposures. METHODS: By using whole-exome sequencing data from matched germline and glioma tumor samples, the authors compared tumor mutational signatures for 17 persons with glioma and a documented occupational history of firefighting with those of 18 persons with glioma without an occupational history of firefighting. All 35 individuals were participants in the University of California, San Francisco Adult Glioma Study. RESULTS: There was a positive correlation among firefighters between the median number of sample variants attributable to single-base substitution signature 42, a single-base substitution mutational signature associated with haloalkane exposure (from the Catalogue of Somatic Mutational Signatures in Cancer) and firefighting years (p = .04; R2 = 0.29). Among nonfirefighters, the individuals with the highest number of median variants attributable to single-base substitution signature 42 also had occupations that possibly exposed them to haloalkanes, such as painting and being a mechanic. CONCLUSIONS: In summary, the authors identified gliomas that had mutational signatures associated with haloalkane exposure that were enriched in firefighters and other occupations.

Humans↗
PubMed1976

The binding of trichlorofluoromethane and other haloalkanes to cytochrome P-450 under aerobic and anaerobic conditions.

1. Trichlorofluoromethane and other haloalkanes interact with hepatic microsomal cytochrome P-450 to give type I spectra under aerobic conditions. 2. Anaerobically, CCl3F, CCl2F. CClF2 and CCl4 interact to give peaks at approx. 420 nm and 455 nm; the other haloalkanes gave peaks at approx. 420 nm only. The formation of the 452 nm peak for CCl3F was time-dependent, and dependent on substrate concentration. 3. Iso-octane extraction of the microsomal preparation increased the magnitude of spectral interaction under reducing conditions but not its rate of formation. Phenobarbitone pretreatment increased the magnitude of the spectral interaction; 3-methylcholanthrene pre-treatment had no effect on the magnitude of the 452 nm peak but decreased its rate of formation. 4. It is suggested that the 452 nm peak represents the interaction of a reactive species formed from CCl3F with the Fe2+ of the haem of reduced cytochrome P-450.

Aerobiosis↗
PubMed1977

Metabolic activation of haloalkanes and tests in vitro for mutagenicity.

1. During incubation of 14CCl4, 14CHCl3, [14C]halothane, or 14CCl3F with liver microsomes and NADPH, considerable radioactivity is bound irreversibly to endoplasmic protein and lipid. However, no 14C was detected in the ribosomal RNA. 2. None of the four haloalkanes studied induced mutations after incubation with liver microsomes and the bacterial tester strains S. typhimurium TA 1535 and TA 1538. 3. Very low or no activity was associated with soluble protein or RNA added to incubation mixtures of the four haloalkanes with liver microsomes.

Animals↗
PubMed1975

A comparative study on the irreversible binding of labeled halothane trichlorofluoromethane, chloroform, and carbon tetrachloride to hepatic protein and lipids in vitro and in vivo.

1) After intraperitoneal injection of labeled CCl4, CHCl3, and halothane in mice, 14C is preferentially bound to liver endoplasmic protein and lipid. A considerable activity is also associated with mitochondrial constituents. Maximal protein binding (nmol/mg): CCl4: 2.8 (0.5 hrs); CHCl3: 11.5 (6 hrs); halothane: 5 (6 hrs). Lipid binding: CCl4: 6.4 (5 min); CHCl3: 8 (4 hrs); halothane: 13.5 (2 hrs). The form of the binding curves in microsomal and mitochondrial protein and lipid differed with the individual haloalkanes. 2) The irreversible (covalent) binding of 14C from labeled haloalkanes in anaerobic suspensions of isolated rabbit liver microsomes and NADPH after 30 min was for protein (lipid) (nmol/mg): CCl4: 15 (58); CHCl3: 3.4 (3.2); halothane: 2.3 (10); trichlorofluoromethane: 6.5 (30). Anerobic incubation favored dehalogenation, but CHCl3 metabolism and irreversible binding requires oxygen. The greatest differences in the in vitro "covalent" binding rates were observed with CHCl3 in rat, mouse, and rabbit. 3) Altered microsomal cytochrome P-450 concentrations in newborn animals, or produced by pretreatment of rats with phenobarbital, 3-methylcholanthrene (MC), or CoCl2 effected similar, but not proportional changes in the rates of irreversible protein and lipid binding. Upon addition of CCl4 the difference of light absorption of reduced liver microsomes from MC-pretreated rats containing cytochrome P-448 appeared at 452 nm. The irreversible binding rate in these microsomes was also increased. The small accleration in irreversible binding in liver microsomes from rats pretreated with isopropanol is not proportional to the high increase of CCl4 toxicity. 4) Practically no binding to added, soluble albumin or RNA was observed in microsomal incubates. However, 14C is bound to the nicotine-adenine dinucleotides of the NADPH system. All haloalkanes produced a similar increase of NADPH oxidation in incubates of rabbit liver microsomes and NADPH.

1-Propanol↗
PubMed1977

Mutagenicity of halogenated alkanes and their derivatives.

The ability of a series of haloalkanes, haloethanols and haloacetaldehydes to induce mutations in Salmonella typhrimurium and preferentially to inhibit the growth of DNA polymerase-deficient E. coli (pol A(+)/pol A(-)) was investigated. For the haloalkanes investigated, the order of reactivities towards the E. coli pol A(+)/pol A(-), was: 1,1,2,2-tetrabromoethane > 1,1-dibromoethane > 1,1,2,2-tetrachlorethane > 1,2-dibromoethane = 1,5 dibromopentane > 1,2-dibromo-2-methylpropane > 1-bromo-2-chloroethane > 1,2-dichloroethane. In the standard Salmonella mutagenicity assay the order of these substances was 1,2-dibromoethane = 1,5-dibromopentane > 1,2-dibromo-2-methylpropane >/= 1-bromo-2-chloroethane > 1,1,2,2-tetrachloroethane = 1,1-dibromoethane > 1,2-dichloroethane. 1,1,2,2-Tetrabromoethane was negative in the standard assay but strongly mutagenic when tested in suspension. It would appear that the discrepancy between the two procedures is due to the fact that bactericidal mutagens cannot be scored reliably in the standard Salmonella assay. The order of reactivity of 2-haloethanols in E. coli pol. A(+)/pol A(-), was 2-iodo > 2-bromo-> 2-chloroethanol. In the Salmonella assay the order was 2-bromo-> 2 iodo- >2-chloro-ethanol. 2-Fluoroethanol and ethanol were devoid of activity in both assays. For the 2-haloacetaldehydes the reactivities in the E. coli system were 2-bromoethylacetate > 2-bromoacetaldehyde = acetaldehyde > 2-chloroacetaldehyde while in the Salmonella system the order was 2-bromoethylacetate > 2-chloroacetaldehyde. Acetaldehyde had minimal activity, while 2-bromoacetaldehyde was without activity but strongly bactericidal.

Acetaldehyde↗
PubMedDate not supplied

Protection by lead nitrate against carbon tetrachloride hepatotoxicity.

Pretreatment with lead nitrate of rats intoxicated with CCl4 exerted a significant protective effect against several damaging effects of the haloalkane. Liver microsomal lipid peroxidation, one of the earliest phenomena in CCl4 intoxication, was clearly inhibited by pretreating the rats with lead. The heavy metal also ameliorated the polyribosomal disaggregation caused by CCl4. Fatty infiltration in the liver, measured by the triglyceride content in the organ, was less pronounced in CCl4-poisoned rats pretreated with lead than in animals treated with the haloalkane alone. Lipid metabolism was also studied by means of Triton WR 1339-induced hypertriglyceridemia to examine the state of triglyceride secretion from liver into plasma; the higher level of plasma triglyceride in the lead-pretreated rats further strengthened the results obtained on the secretion experiments. Finally, CCl4-induced liver necrosis, as measured by serum transaminases and histological examination, was partially prevented by lead. The mechanism by which lead, an inhibitor of the drug-metabolizing enzyme system, interferes with CCl4 intoxication, is disccused.

Alanine Transaminase↗
PubMed1977

Synthesis of phosphonate and ether analogs of rac-phosphatidyl-L-serine.

The chemical synthesis of four phosphonate-containing phosphatidylserine analogs namely, L-serine (+/-)-[2,3-bis(hexadecyloxy) and 2,3-bis(Palmitoyloxy)-propyl] phosphonates, and L-serine (+/-)-[3,4-bis(hexadecyloxy and 3,4-bis(palmitoyloxy)-butyL]phosphonates is descirbed. (+/-)-2,3-Bis(hexadecyloxy) and 2,3-bis(palmitoyloxy)-prophylphosphonic acids and (+/-)-3,4-bis(hexadecyloxy)butylphosponic acid were prepared by reaction of tris(trimethylsily) phosphite on the corresponding haloalkane. Condensation of the above phosphonic acids or (+/-)-3,4-bis(palmitoyloxy)butylphosphonic acid with N-carboxy-L-serine dibenzyl ester in the presence of trichloroacetonitrile or triisopropylbenzenesulfonyl chloride yielded the protected serine intermediates, which on hydrogenolysis gave the desired L-serine analogs. By a similar route, 1,2-dihexadecyl-rac-glycero-3-phosphoric acid was converted to 1,2-dihexadecyl-rac-glycerophospho-L-serine (L-serine (+/-)-2,3-bis(hexadecyloxy)propyl hydrogen phosphate(ester).

Chromatography, Thin Layer↗
PubMed1977

Haloethylene-related compounds of industrial, environmental, and medical significance.

A broad-based literature survey was made for chemicals that contain either a haloethylene or a related substructure. Two hundred and sixty-two compounds, including synthetic intermediates, pesticides, solvents, drugs, food components, natural products, and metabolites, are grouped by their structures. Some are in current use or are bioavailable while little exposure is expected from others. As more biologic-response information is reported for small compounds of these types, it should become possible to select others for research on additional questions of structure-activity relationships. Some of the compounds are widespread while others are not. Some are used or found in large amounts while others may be trace contaminants, minor or more major by-products of synthesis or isolation. The pesticides and solvents, for example, are knowingly and often deliberately released to the environment, sometimes in very large quantities. Inadvertent release also occurs, sometimes referred to as fugitive emission. Food contaminants and drugs are directly accessible to humans. Sparsely distributed natural products could be accessible to humans, for example, via the food chain. Some of the compounds in food may be formed during preparation, storage or metabolically. Last, the haloethylene function has often been synthesized into compounds in order to achieve desired biologic activities. There are many types and degrees of relatedness of structure, depending upon atomic dimensions and stereochemical, polar, resonance, and other factors. Furthermore, for some chemical series, biologic responses are continuously variable while, in other cases, it is not uncommon that qualitatively different types of response occur with apparently very close homologs. Genetic, metabolic, and behavioral factors affecting response must also be considered. Thus, safety or hazard cannot yet be predicted conclusively by apparent relatedness of structure alone. Also, since the tables are noncomprehensive, some relevant compounds have likely been omitted. The haloalkanes, for example, are not here because of their large number, despite the knowledge that some are either metabolized or nonbiologically converted to haloalkenes.

Alcohols↗
PubMed1979

[Interference of antioxidants E/O of some free radical "scavengers" with the activity of glucose-6-phosphatase after administration of carbon tetrachloride].

G-6-Pase activity was investigated in the microsomal fraction from rat liver in the presence of carbon tetrachloride and/or propyl gallate (PG), reduced glutathione (GSH) and superoxide dismutase. Results obtained "in vitro" demonstrated that CCl4 induced a 60% inhibition of the microsomal enzyme activity. Moreover, a marked inhibition of G-6-Pase activity was found also when propyl gallate and reduced glutathione were added, at different concentrations, to incubation mixture. In addition, these drugs were unable to interfere with the dangerous effect exerted on the enzymatic activity by the haloalkane. Additional experiments carried out "in vivo" with propyl gallate produced evidence that intraperitoneal administration of the antioxidant was followed by a significant inhibition of G-6-Pase activity, while the damaging action of CCl4 was unaffected. Some possible explanations of these results are reported.

Animals↗
PubMed1979

[Further investigations on the protective effect of cadmium acetate in bromotrichloromethane poisoning].

The rats were pretreated with cadmium acetate (20 mg/Kg.ip) and subsequently challenged with a dose of bromotrichloromethane (2,6 mmoles/Kg.po), the haloalkane produced no change on liver polyribosomes, as evidenced by disaggregation of sedimentation profile. Cadmium acetate failed to protect against CBrCl3-induced lipid peroxidation, as measured by malonaldehyde production of liver homogenate.

Acetates↗
PubMed1976

CC14 administration to strain A/J mice or rats and the arachidonic acid content of their liver microsomal prospholipids.

CC14 administration of Sprague-Dawley male rats causes a significant decrease in the arachidonic acid content of their liver microsomal phospholipids. On the contrary, its administration to strain A/J male mice does not modify the concentration during periods of intoxication up to 24 hr. Since this strain of mice is more susceptible to CC14-induced injury than the rat, results indicate that lipid peroxidation can not be the key event in damage induced by this haloalkane.

Animals↗