PubMed Health⌕ Search

Biomedical subjects

J B Mailhes

Publications and source records attributed to J B Mailhes.

At least 37 records · Page 2Linked to original sources
PubMed1994

Variation of mouse oocyte sensitivity to griseofulvin-induced aneuploidy and meiotic delay during the first meiotic division.

The effects of varying the time of chemical treatment on the induction of aneuploidy and meiotic delay in metaphase II (MII) oocytes were studied by administering 1,500 mg/kg griseofulvin (GF) at 0, 2, 4, 6, or 8 hr after an injection of human chorionic gonadotrophin (HCG). The results show that the oocytes have a different sensitivity to GF-induced aneuploidy and meiotic delay during the course of meiotic maturation. Although not restricted to a particular period of meiotic maturation, the frequency of aneuploidy was highest (P < 0.05) when GF was given at 2, 4, or 6 hr after HCG. The maximum frequency of hyperploidy (42.4%) occurred at the 4-hr treatment time. Also, GF treatment resulted in the induction of meiotic delay as demonstrated by ovulated metaphase I (MI) and polyploid MII oocytes. The meiotic delay data depict a period of relative resistance between two periods of sensitivity in that the percentages of ovulated MI oocytes were 53.3, 21.3, 3.5, 6.7, and 25.7 when GF was given at 0, 2, 4, 6, and 8 hr after HCG, respectively. Also, at these treatment times the percentages of polyploid oocytes were 0.6, 1.7, 7.7, 20.1, and 15.4, respectively. Therefore, the oocytes seem to be more sensitive to GF-induced meiotic delay during the periods preceding and following meiotic spindle assembly. In conclusion, the results demonstrate that the time of chemical treatment influences the frequency of aneuploidy and the degree of meiotic delay. Also, the results emphasize that to thoroughly characterize the aneugenic potential of a specific chemical several treatment times may be needed.

Aneuploidy↗
PubMed1994

Preferential pericentric lesions and aneuploidy induced in mouse oocytes by the topoisomerase II inhibitor etoposide.

Etoposide (VP-16) is used as an antineoplastic drug in humans. It inhibits topoisomerase II(topoII) activity by forming a ternary complex (DNA-etoposide-topoII). This complex prevents the DNA-strand rejoining activity of topo II, which results in DNA-strand breaks and the formation of structural chromosome aberrations. Topo II activity is also required for removing regions of DNA catenation prior to chromosome segregation. The possibility exists that patients undergoing etoposide chemotherapy may incur genetic damage and, consequently, may be at a greater risk for developing secondary tumors and having genetically abnormal offspring. We studied the ability of etoposide for inducing both structural chromosome aberrations and aneuploidy in mouse oocytes. Different dosages of etoposide were given to female mice at various times before and after human chronic gonadotrophin injection, and ovulated oocytes were collected 17 h later. The proportions of chromatid acentric fragments and of hyperploid metaphase II oocytes were significantly higher (P < 0.01) in the etoposide groups than in concurrent controls. These results indicate that both structural and numerical aberrations can be induced without direct interaction with DNA or with the various organelles associated with chromosome segregation. Additionally, unlike other compounds (vinblastine, colchicine, benomyl, and griseofulvin) that induce both meiotic delay (ovulated metaphase I oocytes and polyploidy) and aneuploidy, etoposide did not cause meiotic delay in oocyte maturation.

Aneuploidy↗
PubMed1994

Comparison of the aneugenic activity of diazepam in mouse oocytes and other mammalian cells.

Previous studies have reported that diazepam (DZ) is capable of inducing mitotic-meiotic arrest and increasing the frequency of aneuploidy in mammalian cells both in vitro and in vivo. We now report that DZ failed to induce either meiotic arrest or aneuploidy in mouse oocytes. In fact, doses of 0, 50, 100, or 150 mg/kg DZ administered at the same time as human chorionic gonadotropin did not induce the ovulation of metaphase I oocytes or of hyperploid metaphase II oocytes. A reduction in the number of ovulated oocytes was observed in the treated groups relative to controls, but this reduction was only significant (p < 0.01) at the highest dose. These findings indicate that different results are found among the assays used for detecting chemically induced aneuploidy. Determining the factors responsible for these differences is an important area for future research.

Aneuploidy↗
PubMed1994

Chemically-induced aneuploidy in mammalian oocytes.

The ability of certain chemicals to elevate the frequency of aneuploidy above spontaneous levels in mammalian experimental models prompts the concern that a similar situation might exist in humans. Validation of experimental models for aneuploidy studies is in progress since there is much to be learned about the causes and mechanisms of chemically-induced aneuploidy. Several biological variables have been shown to influence the results from aneuploidy assays. In this review, we examine these variables as they relate to female germ cell aneuploid assays. Also, we have found that the aneuploidy results obtained from different cell types, sexes, and experimental models cannot necessarily be expected to agree due to certain anatomic and physiologic differences and the end points measured.

Aneuploidy↗
PubMed1994

The influence of postovulatory ageing on the retardation of mouse oocyte maturation and chromosome segregation induced by vinblastine.

Certain compounds can induce ovulated metaphase I (MI) oocytes. To study if these MI oocytes can overcome this blockage, ICR mice were given human chorionic gonadotrophin and 0.6 mg/kg vinblastine sulfate (VBS). Their ovulated oocytes were collected at 17, 19, 21, 23 and 25 h later. The results showed that the frequencies of MI oocytes decreased, the proportions of diploid metaphase II (MII) oocytes increased and the frequencies of hyperploid MII oocytes did not significantly differ (P > 0.05) among the five harvest or postovulatory times. We also found that the proportions of MII oocytes exhibiting premature anaphase II and premature centromere separation increased with postovulatory ageing, and that these frequencies were consistently higher in controls than in the VBS groups. These findings indicate that some of the oocytes blocked in MI can overcome this inhibition and produce primarily diploid MII oocytes. The ultimate fate of ovulated MI and diploid oocytes on aneuploid production hinges upon the formation of a functioning meiotic spindle, which is affected by both dosage and the specific chemical.

Aneuploidy↗
PubMed1993

Investigation of aneuploidy induction in mouse oocytes following exposure to vinblastine-sulfate, pyrimethamine, diethylstilbestrol diphosphate, or chloral hydrate.

The various causative and mechanistic phenomena associated with aneuploidy induction require considerable investigation to better understand the etiology of chromosome missegregation. We investigated the potential of vinblastine sulfate, pyrimethamine, diethylstilbestrol diphosphate, and chloral hydrate to induce numerical and structural chromosome changes in female mouse germ cells. Superovulated ICR mice were administered the compounds either by intraperitoneal injection or oral gavage, and oocytes were collected and processed for cytogenetic analysis 17 hr later. Vinblastine sulfate, administered i.p., induced a significant increase in the frequency of ovulated MI oocytes and of hyperploid MII oocytes compared to controls, but did not increase the frequency of structural aberrations. Pyrimethamine, diethylstilbestrol diphosphate, and chloral hydrate did not increase the frequency of numerical or structural chromosome changes in female mouse germ cells.

Aneuploidy↗
PubMed1993

Griseofulvin-induced aneuploidy and meiotic delay in mouse oocytes: effect of dose and harvest time.

The in vivo mouse oocyte assay provides a useful system for studying both structural and numerical cytogenetic abnormalities induced by chemicals in mammalian germ cells. As part of the development of this assay for investigating chemically-induced numerical chromosome changes, the experimental and biological variables that can influence the outcome of the assay are being determined. In this study, we investigated the effect of griseofulvin (GF) administered by oral gavage on the induction of meiotic delay as measured by ovulated metaphase I (MI) oocytes and the induction of aneuploidy in metaphase II (MII) oocytes. The results indicate that GE significantly increased the frequencies of oocytes blocked in MI and of hyperploid MII oocytes compared to controls. The biological fate of delayed MI oocytes was investigated by harvesting oocytes at different times post treatment. With increasing harvest times, the frequency of MI oocytes decreased and, unexpectedly, the frequency of hyperploid MII oocytes also decreased. This suggests that some MI oocytes can overcome the GF-induced meiotic block, form a normal meiotic spindle, and progress to metaphase II as normal MII oocytes. The significance of these findings for the design and interpretation of in vivo mouse oocyte studies is discussed.

Aneuploidy↗
PubMed1992

The effects of cisplatin on murine metaphase II oocytes.

This study was undertaken to determine if cisplatin can induce aneuploidy in murine oocytes treated prior to ovulation. Control animals were injected with intraperitoneal (ip) saline and the treatment animals were divided into three different dose schedules for ip cisplatin. After ovulation induction, the oocytes were processed for cytogenetic analysis and the chromosomes were counted. There were significantly less oocytes ovulated in the treatment groups when compared to control animals. There was a significant increase in hypohaploid cells counted in the 7.5 mg/kg treatment group, but the percentages of hyperhaploid and polyploid cells were not increased in the treatment groups. The cytogenetic effects of cisplatin in vivo and in vitro are reviewed.

Aneuploidy↗
PubMed1992

Benomyl-induced aneuploidy in mouse oocytes.

Benomyl (methyl-1-[butylcarbamoyl]-2-benzimidazole carbamate) is a plant fungicide which acts by inhibiting tubulin polymerization. It is also a carcinogen and a teratogen. A substantial number of reports consistently show that benomyl inhibits cellular division and induces numerical chromosome changes in somatic cells, while results from standard genotoxicity assays which measure mutations and structural chromosome aberrations are conflicting. To define further the genotoxic effects of benomyl and to demonstrate the utility of the in vivo mouse oocyte assay for detecting chemicals which induce numerical chromosome changes, we investigated the ability of benomyl to induce numerical and structural chromosome aberrations in mouse oocytes. Superovulated female ICR mice were administered benomyl by oral gavage and oocytes were collected 17 h later. The proportions (and percentages) of hyperploid oocytes were 1/309(0.3), 6/155(3.9), 38/229(16.6), 46/130(35.4), 60/215 (27.9), 42/143(29.4) for control, 500, 1000, 1500, 1750 and 2000 mg/kg respectively. No increase in structural aberrations was observed. These results demonstrate that benomyl specifically induces numerical chromosome changes in mouse oocytes.

Aneuploidy↗
PubMed1991

High-risk molar disease.

A retrospective study was undertaken to determine the prevalence of persistent trophoblastic disease among patients with high-risk molar disease. Nineteen patients met the criteria for high-risk molar disease. Fifteen of 19 (71%) patients underwent spontaneous resolution. Four of 19 (21%) developed persistent disease and required chemotherapy.

Adolescent↗
PubMed1990

Cytogenetic analysis of mouse oocytes and one-cell zygotes as a potential assay for heritable germ cell aneuploidy.

Assays are needed for detecting chemically-induced aneuploidy, for investigating the mechanisms of aneuploidy production, and for obtaining heritable germ cell data that can be used to formulate human risk estimates. In this report, we describe the results of experiments designed to study aneuploidy in metaphase II (MII) oocytes induced by intraperitoneal (i.p.) or oral dosages of colchicine, and to investigate the proportion of aneuploid oocytes transmitted to one-cell (1C) zygotes following oral administration of colchicine immediately following HCG. The proportions (and percentages) of hyperploid MII oocytes were: 1/606 (0.2), 37/504 (7.3), 152/731 (20.8) and 75/319 (23.5) for control, 0.2, 0.3 and 0.4 mg/kg, respectively for i.p. administration of colchicine; and 3/216 (1.4), 8/539 (1.5), 81/511 (15.9), 71/398 (17.8) and 98/391 (25.1) for control, 1.0, 2.0, 3.0 and 4.0 mg/kg, respectively for oral administration of colchicine. The proportions of hyperploid 1C zygotes were 2/327 (0.6), 21/389 (5.4), 62/435 (14.3) and 69/438 (15.8) for control, 2.0, 3.0 and 4.0 mg/kg, respectively for oral colchicine. The proportions of hyperploid MII oocytes and 1C zygotes were significantly higher (Chi-square, P less than 0.01) at each i.p. or oral dose (except 1.0 mg/kg oral) than in the controls. The frequencies of hyperploidy induced by oral doses of colchicine were greater in MII oocytes than in 1C zygotes. We also found that the frequency of developmentally delayed and polyploid 1C zygotes increased with the dose of oral colchicine. Developmentally delayed zygotes contained male-derived chromosomes and female-derived fragmented pronuclei and pronuclei with decondensed chromosomes. These results indicate that higher doses of oral colchicine are needed to induce comparable levels of aneuploidy found after i.p. administration, and that aneuploid oocytes are fertilized and reach first cleavage metaphase. In addition, colchicine induces a spectrum of events including aneuploidy, polyploidy and developmentally delayed oocytes and zygotes.

Administration, Oral↗
PubMed1989

An evaluation of uterine scar integrity after cesarean section in rabbits.

Cesarean sections were performed on 30 rabbits at term pregnancy. Two incisions were made in each of the two uterine horns, and each incision was closed according to a predetermined method (continuous, everted; continuous, inverted; interrupted, everted; or interrupted, inverted). Tissue from the uterine scar region was sampled at three different time periods (5-8 days, 12-15 days, or 28-30 days) post-surgery to evaluate the degree of uterine healing by a variety of histologic criteria. The initial healing response in the scarred region occurred around 28-30 days post-surgery. The different uterine closure techniques did not appreciably influence the healing response in this study. We evaluated tensile strength in 36 uterine muscle specimens containing the scar obtained from nine animals in the 28-32-days post-surgery group. Of these 36 specimens, 86.1% tore through the muscle instead of through the scar when tension was applied to the muscle.

Animals↗
PubMed1988

Analysis of mouse metaphase II oocytes as an assay for chemically induced aneuploidy.

Our initial objective was to develop an in vivo mammalian, female aneuploid assay that is consistent, time efficient, and that yields a large number of oocytes amenable to objective analyses. Subsequently, we desired to use such an assay for identifying chemicals and dosages that could increase the incidence of aneuploidy in mouse metaphase II oocytes. The experimental protocol involved superovulating CD-1 mice with PMS; HCG was given 48 h later. At the time of HCG injection, different dosages od diethylstilbestrol diphosphate, cadmium chloride, chloral hydrate, or colchicine were injected intraperitoneally. 17 h later, oocytes were collected and fixed prior to C-banding the chromosomes. The procedure required about 3 h to process oocytes from 25 mice and yielded over 100 analyzable metaphase II oocytes. Colchicine was the only compound tested that resulted in a statistically significant (P less than 0.01) increase in hyperploid (N greater than 20) oocytes over controls. The incidence of hyperploid oocytes in the colchicine group was 2/167, 1/182, 21/220, and 38/202, for control, 0.1 mg/kg, 0.2 mg/kg, and 0.3 mg/kg, respectively. This assay appears sensitive for aneuploidy detection but requires further validation.

Aneuploidy↗
PubMed1988

Morbidity in obese and nonobese patients following gynecologic surgery for cancer.

Meager information exists regarding the morbidity of cancer surgery in obese patients, and it is generally assumed that surgery in the obese patient is attended with increased complications over those found in nonobese patients. A retrospective evaluation was undertaken at the Louisiana State University Medical Center to ascertain the morbidity of cancer surgery among 97 patients. In comparing the obese with the nonobese group of patients, the former was more often found to have complications of postoperative wound disorders that frequently required secondary operations, and a greater incidence of diabetes. The risk of postoperative complications among obese patients undergoing cancer surgery did not otherwise appear to be greater than that of nonobese patients.

Female↗
PubMed1987

Differential sensitivity of mouse oocytes to colchicine-induced aneuploidy.

Unpublished results from our laboratory showed that colchicine increased the incidence of hyperploid mouse metaphase II (MII) oocytes when injected at the same time as human chorionic gonadotrophin (HCG). The objective of the present study was to determine whether the time of administering colchicine influenced the incidence of aneuploidy in MII oocytes. CD-1 mice were given pregnant mare's serum (PMS) and 48 hr later, HCG. An intraperitoneal injection of 0.2 mg/kg colchicine was given at +4, +2, 0, -2, or -4 hr relative to HCG. Oocytes were collected 17 hr post-HCG and processed, and chromosomes were subsequently C-banded. The percentage of hyperploid oocytes was 0.77, 2.56, 5.71, 7.79, 3.54, and 2.70 for control, +4, +2, 0, -2, or -4 hr pre/post-HCG, respectively. Chi-square analyses of these data demonstrated that colchicine significantly increases the proportion of aneuploid oocytes, and that the relative sensitivity of colchicine-induced aneuploidy depends upon the time that this drug is administered relative to HCG.

Aneuploidy↗
PubMed1987

Cytogenetic technique for mouse metaphase II oocytes.

The acquisition of cytogenetic data from mammalian oocytes has required considerable time and expense, since only a relatively small number of oocytes could be processed from three to four animals daily. The availability of a procedure that would facilitate fixation and preparation of air-dried slides from 25-30 superovulated mice within a 3-h period would enhance development of germ cell cytogenetic data by reducing technician time and animal maintenance expense. We present such a procedure for mouse metaphase II oocytes. Mice were superovulated and the oocytes collected were fixed en masse prior to making air-dried slides. Chromosomes were subsequently C-banded to enhance objective cytogenetic analysis. The reliability of the procedure was determined by harvesting 44,814 oocytes from 1,875 mice over a 9-month period and calculating the proportion of cells cytogenetically analyzed to those not analyzed. Cytogenetic analysis of oocytes is an assay for chemicals (and other agents) capable of inducing numerical and structural chromosomal aberrations.

Animals↗
PubMed1987

Aneuploidy determination in C-banded mouse metaphase II oocytes following cyclophosphamide treatment in vivo.

The ability of cyclophosphamide (CYC) to induce aneuploidy in metaphase II oocytes of mice was evaluated. Various dosages (50, 100, 150, 250 and 350 mg/kg body weight) of CYC were injected intraperitoneally prior to induced ovulation. Chromosomes were C-banded to allow a more accurate counting of chromosomes and chromatids, and analysis of structural aberrations. Structural aberrations were not observed. Although the incidence of aneuploid oocytes in the treated groups was greater than that in the control group, the differences were not statistically significant. This result was unlike those of other relevant reports and several plausible explanations for such a disparity are discussed.

Aneuploidy↗