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G S Bailey

Publications and source records attributed to G S Bailey.

134 records · Page 8Linked to original sources
PubMed1969

Phenoxyethanol: protein preservative for taxonomists.

Pieces of chicken heart or skeletal muscle were placed in a dilute solution of the antimicrobial agent 2-phenoxyethanol and stored at room temperature. Under these conditions, the serum albumin, lactate dehydrogenase, and malate dehydrogenase in these tissues survived in easily detectable amounts for at least 2 weeks. The surviving proteins appeared to be identical with those of fresh tissues in physical, catalytic, and immunological properties. Phenoxyethanol also preserved heart and muscle proteins of representatives of other vertebrate classes. Tissue samples collected in the analysis by biochemical taxonomists.

Animals↗
PubMedDate not supplied

The effect of indole-3-carbinol, an aflatoxin B1 hepatocarcinoma inhibitor, and other indole analogs on the rainbow trout hepatic mixed function oxidase system.

Rainbow trout were fed diets containing 3.4 mmol of indole-3-carbinol, indole-3-ethanol, indole-3-aldehyde, or indole-3-acetic acid in 100 g salmon oil/kg diet for 3 weeks. The indoles did not increase hepatic microsomal cytochrome(s) P-450 or P-448 nor induce the associated mixed function oxidase enzyme activities as measured by ethoxyresorufin-O-deethylase (EROD) and benzphetamine-N-demethylase activities. Indole-3-carbinol did not alter the in vitro metabolism of aflatoxin B1 to aflatoxicol and aflatoxin M1; but the other indoles did suppress the formation of aflatoxin M1 from aflatoxin B1. The results suggest that the mechanism by which indole-3-carbinol protected rainbow trout from aflatoxin B1 (AFB1) hepatocarcinogenesis was not via the alteration of the mixed function oxidase system.

Aflatoxin B1↗
PubMedDate not supplied

Neoplasia in zebrafish (Danio rerio) treated with 7,12-dimethylbenz[a]anthracene by two exposure routes at different developmental stages.

Using zebrafish, Danio rerio, initial pioneering work in the 1960s revealed carcinogen responsiveness of fish, yet very few subsequent tumorigenesis investigations have utilized this species. We exposed embryos (60 hours postfertilization) and fry (3 week posthatch) to 7,12-dimethylbenz[a]anthracene (DMBA) by immersion in aqueous solutions for 24 hours, at concentrations of 0-1 or 0-5 ppm (mg/L), respectively. Juvenile zebrafish 2 months posthatch were fed a diet containing 0-1,000 ppm DMBA for 4 months. Fish were sampled for histologic evaluation at 7-12 months after the onset of carcinogen treatment. Fry were most responsive to DMBA and showed the widest diversity of target tissues and histologic types of neoplasia, having several types of epithelial, mesenchymal, and neural neoplasia. The principal target tissues for carcinogenic response were liver following embryo or fry exposure, with gill and blood vessel the second and third most responsive tissues in fry. Intestine was the primary target and gill a secondary target in fish that received dietary DMBA as juveniles. These studies indicate that young zebrafish are most responsive to DMBA, showing a greater diversity of neoplasm types than rainbow trout. Thus, zebrafish are a valuable model system in which to study mechanistic aspects of the carcinogenesis process.

9,10-Dimethyl-1,2-benzanthracene↗
PubMedDate not supplied

Neoplasia in zebrafish (Danio rerio) treated with N-methyl-N'-nitro-N-nitrosoguanidine by three exposure routes at different developmental stages.

We exposed embryos (83 hours postfertilizaton) and fry (3 weeks posthatch) to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) by immersion in aqueous solutions of 0-10 ppm for 1 hour (embryo) or 0-2 ppm for 24 hours (fry). Zebrafish embryos were microinjected with MNNG at levels of 0 or 96 ng/egg. Diets containing 0-2,000 ppm MNNG were fed to juvenile zebrafish for 3 months beginning at 2 months posthatch. Fish were sampled for histopathologic study at 6-12 months after initiation of carcinogen exposure. Embryos and fry were both quite responsive to MNNG; however, juvenile zebrafish were remarkably refractory to MNNG-induced neoplasia. Principal target organs in zebrafish treated as embryos with MNNG were liver and testis, with hepatocellular adenoma the most prevalent hepatic neoplasm. A variety of mesenchymal neoplasms occurred in zebrafish following embryo exposure to MNNG, including chondroma, hemangioma, hemangiosarcoma, leiomyosarcoma, and rhabdomyosarcoma. Testis and blood vessels were primary target organs for MNNG following fry exposure, with seminoma, hemangioma, hemangiosarcoma, and various other epithelial and mesenchymal neoplasms occurring. The zebrafish is a responsive, cost-effective lower vertebrate model system in which to study mechanisms of carcinogenesis.

Animals↗
PubMedDate not supplied

Carcinogenicity of dietary dimethylnitrosomorpholine, N-methyl-N'-nitro-N-nitrosoguanidine, and dibromoethane in rainbow trout.

Eighteen-mo feeding trials of rainbow trout were used to test the carcinogenicity of 5 chemicals in this species. A single exposure level was used for each substance. The doses and chemicals tested were 1,556 ppm 2,6-dimethylnitrosomorpholine (DMNM), 500 ppm N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), 2,000 ppm 1,2-dibromoethane (DBE), 2,000 ppm 1,1-dichloroethylene (DCE), and 200 ppm cyclophosphamide (CP). Liver and/or glandular stomach neoplasms were produced by DMNM (liver and stomach), MNNG (stomach), and DBE (chiefly, stomach tumors). In addition, DMNM produced a low incidence of swimbladder papillomas and caused testicular atrophy in 50% of treated males. DCE and CP produced no neoplasms at the exposure levels used. No evidence of other chronic toxicity was seen for any of the 5 compounds.

Animal Feed↗
PubMedDate not supplied

Indole-3-carbinol and beta-naphthoflavone induction of aflatoxin B1 metabolism and cytochromes P-450 associated with bioactivation and detoxication of aflatoxin B1 in the rat.

Aflatoxin B1 (AFB1) is a highly hepatotoxic and hepatocarcinogenic secondary metabolite of the grain mold Aspergillus flavus and related fungi. Indole-3-carbinol (I3C), found in cruciferous vegetables, can both inhibit and promote AFB1-induced carcinogenesis. We have examined the influence of dietary treatment with I3C and the well-known Ah receptor agonist beta-naphthoflavone (BNF) on the relative levels of different cytochrome P-450 (CYP) isoforms known to metabolize AFB1 in male Fischer 344 rats. After 7 days of feeding 0.2% I3C or 0.04% BNF, alone or in combination, the relative levels of hepatic CYP1A1, 1A2, 2B1/2, 2C11, and 3A were assessed by laser densitometry of Western blots. Both diets containing I3C markedly increased band densities of CYP1A1 (up to 24-fold), 1A2 (3.1-fold), and 3A1/2 (3.8-fold), and had lesser effects on the levels of 2B1/2 (1.8-fold) and no effect on CYP2C11. BNF also strongly increased band densities of CYP1A1 (12-fold) and 1A2 (2.7-fold), but had no effect on the levels of CYP2B1/2 or 3A1/2 band densities, and repressed those of CYP2C11 (2-fold). In addition, we examined the in vitro hepatic microsomal metabolism of AFB1 at 16, 124, and 512 microM substrate levels. Diets containing I3C elevated initial rates of AFM1 (a detoxication product) production 18.6- to 19.2-fold over control at 16 microM AFB1, which declined to 7.8- to 9.5-fold at 512 microM AFB1. The BNF-only diet gave similar, but less dramatic effects (5.9-fold at 16 microM AFB1, 3.5-fold at 512 microM AFB1).(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxin B1↗
PubMedDate not supplied

Indole-3-carbinol induces a rat liver glutathione transferase subunit (Yc2) with high activity toward aflatoxin B1 exo-epoxide. Association with reduced levels of hepatic aflatoxin-DNA adducts in vivo.

Aflatoxin B1 (AFB1), a metabolite of the grain mold Aspergillus flavus, is a potent hepatocarcinogen and widespread contaminant of human food supplies. AFB1-induced tumors or preneoplastic lesions in experimental animals can be inhibited by cotreatment with several compounds, including indole-3-carbinol (I3C), a component of cruciferous vegetables, and the well-known Ah receptor agonist beta-naphthoflavone (BNF). This study examines the influence of these two agents on the AFB1-glutathione detoxication pathway and AFB1-DNA adduction in rat liver. After 7 days of feeding approximately equally inhibitory doses of I3C (0.2%) or BNF (0.04%) alone or in combination, male Fischer 344 rats were administered [3H]AFB1 (0.5 mg/kg, 480 microCi/kg) intraperitoneally and killed 2 hr later. All three experimental diets inhibited in vivo AFB1-DNA adduction (BNF, 46%; I3C, 68%; combined, 51%). Based on Western blots using antibodies specific for the glutathione S-transferase (GST), subunit Yc2 (subunit 10) appeared to be substantially elevated by the diets containing I3C (I3C diet, 4.0-fold increase in band density; combined diet, 2.8-fold). The BNF diet appeared to elevate Yc2 to a lesser extent (2.2-fold increase in band density).(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxin B1↗