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1.
《CMAJ》1968,98(4):221-222
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2.
LSD was found to induce chromosomal aberrations in root tip cells of Allium cepa, Hordeum vulgare and Secale cereale. Aberrations occurred in the form of chromatid and isochromatid breaks with most of these breaks failing to rejoin. The distribution of chromosome breaks was not uniform over the length of chromosomes, and a majority of the breaks were localized at the centromeric regions. For a given dose of LSD (30 g/ml), onion appeared to be more susceptible than barley or rye. The diploid and tetraploid rye used in the study showed no appreciable difference in sensitivity to LSD treatment. — A preliminary study on meiotic chromosomes in LSD-treated diploid rye revealed the presence of univalents, chromosome breaks and fragments, suggesting that LSD can induce meiotic abnormalities in plant material.Contribution from the Department of Agronomy, University of Kentucky. The investigation reported in this paper (73-3-75) is in connection with a project of the Kentucky Agricultural Experiment Station and is published with the approval of the Director.  相似文献   

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In-vitro experiments have been undertaken to assess the effect of ultrasound at diagnostic and therapeutic levels on chromosomes of human lymphocyte cultures. The frequency used was about 2 MHz. The intensity was that of diagnostic level, 23 mW/cm2, which was increased stepwise to 3·5 W/cm2. The time of exposure varied from two to eight hours. No difference could be detected between the numbers of cells with aberrations in the insonated and control cultures, but aggregation of red cells was observed at high intensities.  相似文献   

4.
为了探讨敲除LSD1基因后抑制人慢性髓系白血病 K562细胞增殖的原因,使用前期CRISPR/Cas9技术构建的人慢性髓系白血病 K562 LSD1基因敲除株,通过细胞凋亡Annexin V/PI(碘化丙啶)双染色、细胞PI染色以及流式细胞术技术,探究敲除LSD1基因后,K562细胞的凋亡水平是否改变,细胞周期是否受到影响。结果表明敲除LSD1基因后K562细胞被阻滞在G0/G1期,进入DNA复制期的细胞变少,因此导致细胞增殖速度减慢;通过细胞凋亡Annexin V/PI双染色并分析早期以及晚期凋亡细胞总比例,显示敲除LSD1基因后,不影响K562细胞的凋亡。研究结果表明,敲除LSD1基因后人慢性髓系白血病 K562细胞的增殖受到抑制,这是由于K562细胞增殖周期发生了改变,进入DNA复制期和分裂期的细胞减少;而与细胞凋亡水平的变化无关。  相似文献   

5.
S A Persson 《Life sciences》1977,20(7):1199-1205
Administration of d-lysergic acid diethylamide (LSD) and its analogue 2-bromo lysergic acid diethylamide (BOL) resulted in a shortlasting increase of 3,4-dihydroxyphenylacetic acid (DOPAC) levels in the rat striatum. BOL was more potent than LSD in the dose range 0.5–4.0 mg/kg. Since there was a concomitant increase in the striatal invivo tyrosine hydroxylation as measured by DOPA accumulation after decarboxylase inhibition, our findings suggest that LSD and BOL increase the impulse flow in the nigro-neostriatal pathway probably by central dopamine (DA) receptor antagonism. However, 4 hrs after LSD the DOPAC level was decreased, while the DOPA accumulation was not. Thus the effect of LSD on the dopaminergic system appears not to be limited to a pure receptor antagonism. The possibility also exists that the effect of LSD on the nigro-neostriatal DA pathway is secondary to its effect on the central 5-hydroxytryptaminergic system.  相似文献   

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The effects of extended anaerobic treatments on Vicia faba lateral root-tip chromosomes were determined. It was observed that aberrations resulted from these treatments, and that the frequency varied from root to root as well as from experiment to experiment. It was suggested that the inconsistency observed might be due to variation in the abilities of different roots to produce energy via fermentation routes. If this were true, an inhibition of fermentation would result in a more consistent aberration frequency. A fermentation inhibitor, NaF, was used in combination with extended anaerobic treatments. The observed frequency of aberrations after the combined treatments was generally higher and considerably less variable. Although other hypotheses might account for the NaF effect, the hypothesis most compatible with the evidence is that the effect is due to energy deprivation. The experimental results are discussed in terms of the aforementioned effect and in terms of three alternative hypotheses for the production of chromosomal aberrations as a consequence of a lack of energy. It is concluded that damage might result from a build-up of normal cellular compounds to abnormally high concentrations which would act directly or indirectly on the chromosomes, from the breakdown of DNA as an energy source, or simply as a result of the fact that the chromosome needs energy to remain intact.  相似文献   

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A number of positive and negative studies have been reported with regard to the damaging effects of LSD on human chromosomes. The present report describes a comparative study of cytogenetic analyses of 200 metaphases of lymphocytes from each of 6 subjects (3 males, 3 females) at varying concentrations of LSD, along with a positive control with mitomycin C and a negative control with sterile water. Results of a small pilot study on the effects of LSD on growth, macromolecular synthesis, mutation, and recombination in bacteria, λ phage and mammalian cells are also included. The data failed to show any significant differences between chromosome aberrations and LSD. Significant changes in somatic cells and in chromosomes occurred only at high doses of LSD.  相似文献   

12.
The combined treatment of cultures of human embryonic lung cells with herpes simplex virus type 2 and cytosine arabinoside produced a significantly increased number of cells containing multiple chromatid and chromosome breaks. The incidence of such cells was found to be approximately two and one half times greater than the additive effects of virus and cytosine arabinoside induced separately and is therefore synergistic.  相似文献   

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早熟凝集染色体和诱导凝集的染色体扫描电镜研究   总被引:1,自引:0,他引:1  
潘岛  刘凌云 《遗传学报》1996,23(6):425-430
应用细胞融合技术和扫描电镜研究了BK(牛肾)细胞早熟凝集染色体(PCC)和诱导PCC的CHO中期染色体的超微结构。所用电镜标本制备方法,尽可能使之减少人工效应,故首次观察到PCC超微结构,特别是早、中、晚S-PCC超微结构的自然状态,从早、中、晚S-PCC的染色体片段所显示的PCC的多级亚结构,进一步了解了BK细胞染色体的超微结构。诱导PCC的CHO中期染色体表面显示出整齐的小毛样由螺旋纤维形成的环状突起。  相似文献   

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Intralocus sexual conflict and intragenomic conflict both affect sex chromosome evolution and can in extreme cases even cause the complete turnover of sex chromosomes. Additionally, established sex chromosomes often become the focus of heightened conflict. This creates a tangled relationship between sex chromosomes and conflict with respect to cause and effect. To further complicate matters, sexual and intragenomic conflict may exacerbate one another and thereby further fuel sex chromosome change. Different magnitudes and foci of conflict offer potential explanations for lineage-specific variation in sex chromosome evolution and answer long-standing questions as to why some sex chromosomes are remarkably stable, whereas others show rapid rates of evolutionary change.Compared to the autosomes, the unique inheritance pattern of the sex chromosomes is often thought to intensify evolutionary conflict (Rice 1984; Frank 1991; Jaenike 2001). Sex chromosomes are therefore hot spots for two specific types of conflict: intralocus conflict, in which an allele confers different fitness effects depending on the sex in which it is found, and intragenomic conflict, in which selfish genetic elements (SGEs) promote their own transmission at the expense of unlinked regions of the genome. These conflicts act in distinct but complementary ways. Not only do they shape sex chromosome and genome evolution, but in some cases, they also have the power to cause complete turnover of sex chromosomes.Unlike the autosomes, because the sex chromosomes are unevenly transmitted between males and females and are also unevenly distributed between the sexes (Fig. 1), the relative effect of male- and female-specific selection acting on them is unbalanced. The inherent differences in sex-specific selection on the sex chromosomes themselves, and between the sex chromosomes and the autosomes, form the basis of a large and often compelling body of evolutionary theory that predicts the ways that intralocus sexual conflict will arise, play out, and in some cases potentially be resolved. This theory predicts that, under some conditions, the sex chromosomes are hot spots of intralocus sexual conflict (Rice 1984; Albert and Otto 2005; Connallon and Clark 2010), and in some cases alleles that harm one sex more than they benefit the other can still reach high frequencies if they are sex-linked (Rice 1984; Dean et al. 2012). All this theory predicts that although the sex chromosomes generally represent a small proportion of the genome, they should play a disproportionately large role in sexual conflict, sexual dimorphism, and sexual selection. There is substantial empirical evidence supporting at least some of this theory (Dean and Mank 2014).Open in a separate windowFigure 1.Transmission of the sex chromosomes. Females are shown in red, males in blue. In male heterogamety (A), the Y chromosome is passed through the patriline and limited to males. The maternal X chromosome is passed from mother to both sons and daughters, but the paternal X can only be transmitted to daughters. Additionally, the X is present two-thirds of the time in females. In female heterogamety (B), the W chromosome is limited to females and passed solely from mother to daughter. The paternal Z chromosome can be passed from father to both daughters and sons; however, the maternal Z chromosome is only passed to sons. Converse to the X chromosome, the Z chromosome is resident in males two-thirds of the time.

Table 1.

Studies showing a disproportionate role of the sex chromosomes in sexual dimorphism, fitness, or fertility
Male heterogametyFemale heterogamety
X chromosomeY chromosomeZ chromosomeW chromosome
Associations with sexually dimorphic phenotypic traitsSize dimorphism in red deer (Foerster et al. 2007)
Sexually antagonistic fitness variation in Drosophila (Gibson et al. 2002; Innocenti and Morrow 2010)
Variation in stalk-eyed fly eye span (Wolfenbarger and Wilkinson 2001)
Male coloration in guppies (Winge 1927; Postma et al. 2011)
Male mating behavior in sticklebacks (Kitano et al. 2009; although see Natri et al. 2013)
Female mating preference in moths (Iyengar et al. 2002)
Female mate choice in flycatchers (Saether et al. 2007)
Male plumage traits in flycatchers (Saetre et al. 2003)
Female benefit coloration in cichlids (Roberts et al. 2009)
Associations with reproduction and fertilityMale reproductive genes in mice (Mueller et al. 2008)Male fertility genes in mammals (Lange et al. 2009)
Male fitness in Drosophila (Lemos et al. 2010; Sackton et al. 2011)
Genes related to male reproductive function in silk moth (Arunkumar et al. 2009)Genes related to female fecundity and fertility in chickens (Moghadam et al. 2012)
Open in a separate windowIn addition to their role in sexual conflict, the sex chromosomes also experience high levels of intragenomic conflict resulting from SGEs that promote their own transmission at the expense of the rest of the genome (Burt and Trivers 2006). Of particular importance are sex-linked segregation distorters, as these generate strong selection favoring genes that suppress their action. Theory predicts that intragenomic conflict should be particularly intense when involving the sex chromosomes (Hurst and Pomiankowski 1991). This is because sex chromosomes can generate antagonistic coevolution between sex-linked segregation distorters and their suppressors (Partridge and Hurst 1998).In addition to shaping the evolutionary properties of existing sex chromosomes, in some situations sexual and intragenomic conflict may also actually catalyze the formation of sex chromosomes (Fisher 1931; Charlesworth and Charlesworth 1980; Rice 1987; Werren and Beukeboom 1998). Conflict may also explain the rate of degradation of the sex-limited Y and W chromosomes (Bachtrog et al. 2011) and turnover of sex chromosomes (Hall 2004; van Doorn and Kirkpatrick 2007, 2010), suggesting that conflict plays a causal role in sex chromosome evolution.There is also growing evidence of a direct relationship between SGEs and sexual conflict involving the sex chromosomes. Many SGEs increase their transmission advantage by targeting sperm, which can reduce male fertility owing to reduced overall sperm production. Lower sperm production can in turn result in reduced siring success during sperm competition (Price and Wedell 2008) and potentially favor polyandry as a female strategy to bias paternity against SGE-carrying males (Wedell 2013). As a consequence, SGEs may also influence the potential for sexual conflict as they can favor increased female mating rates, which increases the potential for conflict between the sexes.Sexual and intragenomic conflict are therefore critical for sex chromosome evolution and, once sex chromosomes are established, can further shape their evolutionary and genomic properties. Disentangling cause and effect is difficult but crucial to understanding the role of sex chromosomes in sexual and intragenomic conflict and vice versa.  相似文献   

18.
The structure of synaptonemal complexes (SCs) of chromosomes of mouse primary spermatocytes were studied using electron microscopy on days 1, 10, and 36 after the completion of per os administration of drugs belonging to three groups of antibiotics: tetracyclins, macrolides, and fluoroquinolones. The antibiotics were administered to mice during ten days. At the substages of early and middle pachytene, heteromorphic SC bivalents and fragments of chromosome-core elements were detected in spermatocytes at all times studied after the administration of the antibiotics of three groups. As cells passed through the period from early to middle pachytene, the number of cells containing heteromorphic SC bivalents and the fragments of axial cores gradually decreased, which could be an indication of selection of cells with chromosomal aberrations. A high level of associations between the X chromosome and autosome bivalents (including heteromorphic ones) also favors this suggestion. A gradual decrease in the number of chromosomal aberrations was detected, as time elapsed from the completion of antibiotics administration. The study of sperm obtained from epididymises of males did not reveal significant differences in both morphology and motility of sperm between males of the control and experimental groups.  相似文献   

19.
It is shown that under the influence of an autosomal meiotic mutant that causes abnormalities in meiotic centromere function (mei-S332), ring-X chromosomes are frequently nonrecoverable. Evidence is presented that this nonrecoverability is caused by a failure of sister ring-chromatids to successfully effect an equational separation with resultant dominant lethality. Because mei-S332 results in meiotic abnormalities only after replication has been completed, and because ring chromosomes are normally transmitted with approximately the same efficiency as rod chromosomes, it is suggested that during replication in normal meioses, sister ring-chromatids form mutually interlocked ring complexes that are resolved without genetic consequences at anaphase II, with the resolution owing at least in part to normal centromere function.  相似文献   

20.
M E Trulson  B L Jacobs 《Life sciences》1979,24(22):2053-2061
Repeated administration of LSD to rats (100 μg/kg every 6 hours for 4 days) resulted in significant decreases in both the KD (?17 &; ?23%) and Bmax (?25 %&; ?30%) for [3H]—5HT binding in forebrain and brainstem plus spinal cord. [3H] — LSD binding showed significant changes in Bmax values (?19%) in forebrain and brainstem plus spinal cord, while KD values were not significantly changed. Neither a single injection of LSD (100 μg/kg) nor repeated administration of brom-LSD (100 μg/kg every 6 hours for 4 days) produced any significant changes in binding. In addition, repeated LSD administration produced no significant changes in [3H] — spiroperidol binding.  相似文献   

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