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51.
Nesnow S; Davis C; Nelson G; Ross JA; Allison J; Adams L; King LC 《Carcinogenesis》1997,18(10):1973-1978
C3H10T1/2CL8 (C3H10T1/2) mouse embryo fibroblasts were used to study the in
vitro carcinogenic activities of dibenzo[a,l]pyrene (DB[a,l]P) and
benzo[a]pyrene (B[a]P). The morphological transforming activities of these
rodent carcinogens were compared using replicate concentration- response
studies. In concentration ranges where both polycyclic aromatic
hydrocarbons (PAHs) were active, DB[a,l]P proved to be four to 12 times as
potent as B[a]P based on concentration. At lower concentrations DB[a,l]P
was active at 0.10 and 0.20 microM, concentrations where B[a]P was
inactive. This makes DB[a,l]P the most potent non-methylated PAH evaluated
to date in C3H10T1/2 cells. DNA adducts of DB[a,l]P in C3H10T1/2 cells were
analyzed by both TLC and TLC/HPLC 32P-postlabeling methods using
mononucleotide 3'-phosphate adduct standards derived from the reactions of
anti-DB[a,l]P-11,12-diol- 13,14-epoxide (anti-DB[a,l]PDE) and
syn-DB[a,l]P-11,12-diol-13,14- epoxide (syn-DB[a,l]PDE) with deoxyadenosine
3'-monophosphate and deoxyguanosine 3'-monophosphate. All of the DNA
adducts observed in C3H10T1/2 cells treated with DB[a,l]P were identified
as being derived from the metabolism of DB[a,l]P to its fjord region diol
epoxides through DB[a,l]P-11,12-diol. The predominant adduct was identified
as an anti-DB[a,l]PDE-deoxyadenosine adduct. Other major adducts were anti-
DB[a,l]PDE-deoxyguanosine and syn-DB[a,l]PDE-deoxyadenosine adducts with
minor amounts of syn-DB[a,l]PDE-deoxyguanosine adducts. These DNA adduct
data are consistent with similar findings of DB[a,l]PDE- deoxyadenosine
adducts in mouse skin studies and human mammary cells in culture.
相似文献
52.
Assessment of the mutagenicity of dichloroacetic acid in lacI transgenic B6C3F1 mouse liver 总被引:2,自引:0,他引:2
Dichloroacetic acid (DCA) is a chlorination byproduct found in finished
drinking water. When administered in drinking water this chemical has been
shown to produce hepatocellular adenomas and carcinomas in B6C3F1 mice over
the animal's lifetime. In this study, we investigated whether mutant
frequencies were increased in mouse liver using treatment protocols that
yielded significant tumor induction. DCA was administered continuously at
either 1.0 or 3.5 g/l in drinking water to male transgenic B6C3F1 mice
harboring the bacterial lacI gene. Groups of five or six animals were
killed at 4, 10 or 60 weeks and livers removed. At both 4 and 10 weeks of
treatment, there was no significant difference in mutant frequency between
the treated and control animals at either dose level. At 60 weeks, mice
treated with 1.0 g/l DCA showed a 1.3-fold increase in mutant frequency
over concurrent controls (P = 0.05). Mice treated with 3.5 g/l DCA for 60
weeks had a 2.3-fold increase in mutant frequency over the concurrent
controls (P = 0.002). The mutation spectrum recovered from mice treated
with 3.5 g/l DCA for 60 weeks contained G:C-->A:T transitions (32.79%)
and G:C-->T:A transversions (21.31%). In contrast, G:C-->A:T
transitions comprised 53.19% of the recovered mutants among control
animals. Although only 19.15% of mutations among the controls were at T:A
sites, 32.79% of the mutations from DCA-treated animals were at T:A sites.
This is consistent with the previous observation that the proportion of
mutations at T:A sites in codon 61 of the H-ras gene was increased in
DCA-induced liver tumors in B6C3F1 mice. The present study demonstrates
DCA-associated mutagenicity in the mouse liver under conditions in which
DCA produces hepatic tumors.
相似文献
53.
54.
55.
Identification of differentially expressed genes in aflatoxin B1- treated cultured primary rat hepatocytes and Fischer 344 rats 总被引:4,自引:1,他引:4
Harris AJ; Shaddock JG; Manjanatha MG; Lisenbey JA; Casciano DA 《Carcinogenesis》1998,19(8):1451-1458
Aflatoxin B1 (AFB1), a mutagen and hepatocarcinogen in rats and humans, is
a contaminant of the human food supply, particularly in parts of Africa and
Asia. AFB1-induced changes in gene expression may play a part in the
development of the toxic, immunosuppressive and carcinogenic properties of
this fungal metabolite. An understanding of the-role of AFB1 in modulating
gene regulation should provide insight regarding mechanisms of AFB1-induced
carcinogenesis. We used three PCR- based subtractive techniques to identify
AFB1-responsive genes in cultured primary rat hepatocyte RNA: differential
display PCR (DD-PCR), representational difference analysis (RDA) and
suppression subtractive hybridization (SSH). Each of the three techniques
identified AFB1- responsive genes, although no individual cDNA was isolated
by more than one technique. Nine cDNAs isolated using DD-PCR, RDA or SSH
were found to represent eight genes that are differentially expressed as a
result of AFB1 exposure. Genes whose mRNA levels were increased in cultured
primary rat hepatocytes after AFB1 treatment were corticosteroid binding
globulin (CBG), cytochrome P450 4F1 (CYP4F1), alpha-2 microglobulin,
C4b-binding protein (C4BP), serum amyloid A-2 and glutathione S-transferase
Yb2 (GST). Transferrin and a small CYP3A-like cDNA had reduced mRNA levels
after AFB1 exposure. Full-length CYP3A mRNA levels were increased. When
liver RNA from AFB1-treated male F344 rats was evaluated for transferrin,
CBG, GST, CYP3A and CYP4F1 expression, a decrease in transferrin mRNA and
an increase in CBG, GST, CYP3A and CYP4F1 mRNA levels was also seen.
Analysis of the potential function of these genes in maintaining cellular
homeostasis suggests that their differential expression could contribute to
the toxicity associated with AFB1 exposure.
相似文献
56.
B. Guigas J. E. de Leeuw van Weenen N. van Leeuwen A. M. Simonis‐Bik T. W. van Haeften G. Nijpels J. J. Houwing‐Duistermaat M. Beekman J. Deelen L. M. Havekes B. W. J. H. Penninx N. Vogelzangs E. van ‘t Riet A. Dehghan A. Hofman J. C. Witteman A. G. Uitterlinden N. Grarup T. Jørgensen D. R. Witte T. Lauritzen T. Hansen O. Pedersen J. Hottenga J. A. Romijn M. Diamant M. H. H. Kramer R. J. Heine G. Willemsen J. M. Dekker E. M. Eekhoff H. Pijl E. J. de Geus P. E. Slagboom L. M. ‘t Hart 《Diabetic medicine》2014,31(8):1001-1008
57.
58.
Ante Prki? Christiaan JA van Bergen Bertram The Denise Eygendaal 《World journal of orthopedics》2016,7(1):44-49
The elbow joint is a complex joint, which, when impaired in function, leads to severe disability. In some cases however, an arthroplasty might be an appropriate treatment. In the past four decades, large steps havebeen taken to optimize this treatment in order to achieve better post-operative outcomes. To understand these progresses and to discover aspects for upcoming improvements, we present a review on the past developments, the present state of affairs and future developments which may improve patient care further. 相似文献
59.
60.
Nienke R Biermasz Alberto M Pereira Jan W A Smit Johannes A Romijn Ferdinand Roelfsema 《Growth hormone & IGF research》2005,15(3):200-206
OBJECTIVE: Depot formulations of somatostatin analogues are increasingly used in the treatment of active acromegaly. A priori knowledge of the efficacy of these drugs in controlling GH excess is clinically relevant, because only approximately 60% of the patients respond with adequate control of GH (GH levels < 5 mU/L) and/or IGF-1 levels upon this treatment. Therefore, we assessed the acute responses of serum GH levels to a new octreotide test (intravenous administration of 50 microg) in 98 consecutive patients with active acromegaly and we measured the predictive value of this test for the efficacy of chronic octreotide-long acting repeatable (octreotide-LAR) treatment in 18 patients. DESIGN: Serum GH concentrations were measured before and at 20, 30, 45, 60, 90, 120, 150 and 180 min following 50 microg i.v. octreotide. The minimal achieved GH was used for analysis. Octreotide-LAR was individually titrated aiming at a normal serum IGF-I for age and a serum GH < 5 mU/L. The mean of 3-6 monthly serum GH and IGF-I measurements after individual dose adjustment was used for evaluating the efficacy of chronic therapy. RESULTS: Octreotide decreased GH levels to values below 5 mU/L in only 49% of unselected consecutive patients and the response was inversely related to basal GH levels. In patients with baseline GH above 50 mU/L, 50 microg i.v. octreotide reduced GH to < 5 mU/L in only 15% of cases (n = 41), whereas in patients with baseline GH levels below 50 mU/L this goal was achieved in 77% of cases. The fractional decrease in GH levels upon octreotide injection was similar in microadenomas and macroadenomas. The minimally achieved serum GH concentration during the intravenous octreotide test was a good predictor for the GH concentrations during long-term octreotide-LAR treatment as assessed in 18 patients. The intravenous octreotide test, using a minimal GH level of < 5 mU/L, had a sensitivity, positive and negative predictive value of 100% for prediction of GH suppression to below 5 mU/L during long term octreotide-LAR treatment. For predicting the response of IGF-I during long-term treatment, the test performed with a sensitivity of 73% and a positive predictive value of 73%. CONCLUSION: Intravenous octreotide reduces GH to concentrations < 5 mU/L in approximately 50% of consecutive patients with active acromegaly, which predicts a good response to chronic octreotide-LAR treatment. 相似文献