油松花粉遗传毒性研究

目的 探讨油松花粉的遗传毒性,为其应用提供安全性毒理学评价依据.方法 用鼠伤寒沙门细菌营养缺陷型突变株TA97(a)、TA 98、TA 100和TA 102,采用平皿掺入法进行Ames实验,将实验分为加和不加代谢激活系统S9 2组平行实验.受实物设5个剂量组(0.008、0.040、0.200、1.000、5.000 mg/皿).应用小鼠骨髓嗜多染红细胞微核实验,检测小鼠骨髓嗜多染红细胞微核率;利用小鼠精子畸形实验,观察不同浓度的油松花粉致小鼠精子畸形的数目.结果 在Ames实验中,油松花粉各剂量组引起的回变菌落数未超过对照组自发回变菌落数的1倍以上;小鼠骨髓嗜多染红细胞微核实验显示,油松花粉3个剂量组的微核发生率均在正常范围内,与阴性对照组比较差异无显著性(P＞0.05),与阳性对照组比较差异显著(P＜0.05);小鼠精子畸形实验显示,油松花粉3个剂量组的精子畸形率均在正常范围内,与阴性对照组比较差异无显著性(P＞0.05),与阳性对照组比较差异显著(P＜0.05).结论 油松花粉对所实菌株、小鼠体细胞及生殖细胞无诱变性.     

土木香水煎液急性毒性和遗传毒性的研究CSCD

目的探讨土木香水煎液的急性毒性和遗传毒性,为土木香临床安全应用提供实验依据。方法采用最大耐受剂量法评价土木香水煎液的急性毒性,观察小鼠体重变化,心、肝、脾和肾的脏器指数变化;采用精子畸形实验,微核实验和彗星实验评价土木香水煎液的遗传毒性。将小鼠随机分为阴性对照组、阳性对照组和土木香水煎液高、中、低剂量组(分别灌胃蒸馏水,40 mg/kg·bw环磷酰胺,40、20、10 g/kg·bw土木香水煎液)。用药后取附睾制成精细胞悬液观察畸形精子数量。取骨髓细胞观察嗜多染红细胞的微核率。取肝、胸腺和脾细胞观察土木香水煎液对小鼠DNA的损伤。结果土木香水煎液经口给药小鼠最大耐受剂量为80 g/kg·bw,该剂量对小鼠的体重及各脏器指数无明显影响与阴性对照组比较差异无统计学意义(P>0.05)。高和中剂量组的精子畸形率明显高于阴性对照组(P<0.05),低剂量组精子畸形率与阴性对照组比较,差异无统计学意义(P>0.05)。高剂量组的微核率明显高于阴性对照组,与之比较差异有统计学意义(P<0.05),而中和低剂量组与阴性对照组比较,差异无统计学意义(P>0.05)。各剂量组肝细胞、胸腺及脾细胞头尾DNA百分比、尾长、尾矩及Olive尾矩与阴性组比较差异无统计学意义(P>0.05)。结论土木香的最大耐受计量为80 g/kg,属于无毒级。高和中剂量的土木香水煎液对生殖细胞有一定的毒性作用,且高剂量有潜在的遗传毒性。     

流式细胞仪检测小鼠骨髓嗜多染红细胞微核率方法的改进

目的观察经γ射线照射后不同时相点小鼠骨髓嗜多染红细胞微核率的变化,进一步完善微核流式细胞仪自动化检测方法。方法 ICR雄性小鼠给予60Coγ射线一次性全身照射,每组4只,剂量分别为1.0、3.0和6.0 Gy,与照射后0.5、2、6和12 h取材;阴性对照组给予假照射;阳性对照组注射环磷酰胺24 h后取材。结果 1.0 Gyγ射线照射后6 h,骨髓f MNPCE显著升高(P<0.01);而3.0 Gy及6.0 Gy照射后6 h,骨髓f MNPCE显著升高(P<0.01);2种方法检测结果显示均有较好的剂量、时间依赖性,并呈显著正相关性(r=0.962,P<0.05)。结论红细胞微核流式细胞仪自动化检测方法快速、简单、灵敏、客观,完全适用于小鼠骨髓红细胞微核率的检测。     

土木香水煎液急性毒性和遗传毒性的研究

目的探讨土木香水煎液的急性毒性和遗传毒性,为土木香临床安全应用提供实验依据。方法采用最大耐受剂量法评价土木香水煎液的急性毒性,观察小鼠体重变化,心、肝、脾和肾的脏器指数变化;采用精子畸形实验,微核实验和彗星实验评价土木香水煎液的遗传毒性。将小鼠随机分为阴性对照组、阳性对照组和土木香水煎液高、中、低剂量组(分别灌胃蒸馏水,40 mg/kg·bw环磷酰胺,40、20、10 g/kg·bw土木香水煎液)。用药后取附睾制成精细胞悬液观察畸形精子数量。取骨髓细胞观察嗜多染红细胞的微核率。取肝、胸腺和脾细胞观察土木香水煎液对小鼠DNA的损伤。结果土木香水煎液经口给药小鼠最大耐受剂量为80 g/kg·bw,该剂量对小鼠的体重及各脏器指数无明显影响与阴性对照组比较差异无统计学意义(P0.05)。高和中剂量组的精子畸形率明显高于阴性对照组(P0.05),低剂量组精子畸形率与阴性对照组比较,差异无统计学意义(P0.05)。高剂量组的微核率明显高于阴性对照组,与之比较差异有统计学意义(P0.05),而中和低剂量组与阴性对照组比较,差异无统计学意义(P0.05)。各剂量组肝细胞、胸腺及脾细胞头尾DNA百分比、尾长、尾矩及Olive尾矩与阴性组比较差异无统计学意义(P0.05)。结论土木香的最大耐受计量为80 g/kg,属于无毒级。高和中剂量的土木香水煎液对生殖细胞有一定的毒性作用,且高剂量有潜在的遗传毒性。     

桉叶油毒性及其对环磷酰胺致小鼠骨髓微核及精子畸形的保护作用

目的探讨桉叶油对环磷酰胺(CP)致小鼠遗传毒性的保护作用。方法①毒性实验:小鼠ig给予桉叶油1700,1750,1800,1850和1900mg·kg-1,检测桉叶油的半数致死量(LD50)。另小鼠分别ig给予桉叶油100,200和400mg·kg-1及花生油(阴性对照)组,每天1次,连续5d。阳性对照组ip给予CP40mg·kg-1,每天1次,共给2d。检测小鼠骨髓嗜多染红细胞微核率。30只雄性小鼠,分别ig给予按叶油100,200和400mg·kg-1和花生油,阳性对照组ip给予CP40mg·kg-1,每天1次,连续5d。观察小鼠精子畸形率。②保护作用实验:小鼠按照如下分组给药:CP+桉叶油400,200和100mg·kg-1,花生油+CP,CP组。第4天与阳性对照组一起ip给予CP40mg·kg-1,每天1次。第5天给药后测定小鼠骨髓微核率。30只雄性小鼠按分组,第6天起与阳性对照组一起每天ip给予CP40mg·kg-1,连续5d,实验共10d。测定小鼠精子畸形率。结果①毒性实验:桉叶油的LD50为1824.01mg·kg-1,95%可信限为(1799.48～1851.19)mg·kg-1。桉叶油对小鼠骨髓嗜多染红细胞微核率和精子畸形率无影响。②保护作用实验:桉叶油100,200和400mg·kg-1组的微核率和精子畸形率明显低于未ig给予桉叶油的CP诱发的微核率和精子畸形率(P<0.05)。结论桉叶油对小鼠无明显的遗传毒性,可降低CP所致小鼠骨髓嗜多染红细胞微核率和精子畸形率。     

低纯度熊果酸对小鼠致变性及其拮抗作用的研究

目的研究熊果酸(Ursolic Acid,UA)的致突变作用及其拮抗作用。方法采用小鼠骨髓嗜多染红细胞微核实验、小鼠染色体畸变实验、小鼠精子畸形实验和改进的小鼠骨髓嗜多染红细胞微核实验、染色体畸变实验、小鼠精子畸形实验,通过检测骨髓嗜多染红细胞微核率、染色体畸变率和精子畸形率来研究熊果酸的致突变性和抗突变性。结果熊果酸各致突变实验组(HUA、MUA、LUA)与阳性对照组(环磷酰胺,CP)相比,差异有统计学意义(P0.05),表明熊果酸没有致突变性;熊果酸抗突变实验组(HUA+CP、MUA+CP和LUA+CP)与阳、阴性对照组相比,差异有统计学意义(P0.05),表明熊果酸可降低环磷酰胺诱发的细胞微核、染色体畸变率和精子畸形率。结论在本试验条件下,熊果酸无致突变作用,具有一定的拮抗作用。     

苦参碱口服给药对小鼠精子活性的影响

目的探讨苦参碱体内对小鼠精子活性、精子密度、畸形发生率,以及对雌性小鼠受孕情况的影响。方法50只NIH雄性小鼠随机分成5组,分别为空白对照组、供试品苦参碱设低、中、高3个剂量组,分别灌胃给予2、4、8mg.kg-1和醋酸棉酚20 mg.kg-1阳性对照组。连续灌胃给药21d后,各组雄性小鼠分别与10只NIH雌性小鼠合笼5d后再分笼(合笼及分开饲养期间雄性小鼠持续给药),分笼5 d后脱颈椎处死各组雄性小鼠,观察并计算精子活性、精子密度及畸形发生率。分笼后第十天解剖、观察并计数雌鼠怀孕胎数。结果苦参碱给药组及阳性对照组精子活性与空白对照组相比较均有显著差异(P<0.05),畸形发生率有显著差异(P<0.01),各给药组、阳性对照组在短时间内(31d)与空白对照组相比,精子密度和雌性小鼠受孕胎数均未产生显著的影响(P>0.05).结论苦参碱口服给药后对小鼠精子活性有一定抑制作用且具有明显的致畸作用。     

红豆杉茎叶毒理学研究

目的:观察红豆杉茎叶的安全性。方法:急性毒性试验采用最大耐受剂量法。遗传毒性试验中Ames试验采用常规平板掺入法;骨髓细胞微核试验以小鼠取胸骨制片镜检;小鼠精子畸形试验以雄性小鼠取双侧附睾制片镜检。大鼠30d喂养试验取断乳SD大鼠,连续观察30d,观察体质量生长状况、饲料消耗及利用率、血液生化检查、脏器质量及病理组织学检查。结果:小鼠经口MTD>10.0g·kg-1,属实际无毒级;Ames试验中的各浓度下,无论是否加入S9混合液,回变菌落数均未大于自发回变数的2倍,并且未见剂量-反应关系。而各阳性对照组均显示强烈的诱变作用;在骨髓细胞微核试验中,试验组动物在各试验剂量下,嗜多染红细胞(PCE)微核出现率、PCE/成熟红细胞(RBC)与阴性对照组相比,差异均无显著性(P>0.05),而阳性对照组与阴性对照组相比,差异有显著性(P<0.05),显示强烈的致突变作用;在小鼠精子畸形试验中,阴性对照组的精子畸形率为1.98%,阳性对照组的精子畸形率为5.24%,与阴性对照组相比差异有显著性(P<0.05),而试验3个剂量组的精子畸形率分别为2.04%,2.00%,2.08%,与阴性对照组相比差异无显著性(P>0.05);大鼠30d喂养试验结果表明,与对照组比较,红豆杉茎叶3个剂量组大鼠的一般情况、体质量、食物利用率、血液学、血液生化学、脏体比及病理组织学检查均未见异常。结论:红豆杉茎叶属实际无毒级,未见遗传毒性,长期服用是安全的。     

柠檬酸包埋的四氧化三铁纳米颗粒的安全性研究

目的对直径为15 nm的柠檬酸包埋的四氧化三铁纳米颗粒(下以Fe3O4-CA表示)进行安全性研究.方法将Fe3O4-CA以等体积不等浓度经口染毒,分别进行小鼠最大耐受量试验,小鼠骨髓细胞微核试验,小鼠精子畸形试验.结果小鼠灌胃最大耐受量大于600 mg*kg-1;小鼠骨髓细胞微核试验,各剂量组的微核率均低于0.2%;小鼠精子畸形试验中,Fe3O4-CA高剂量组小鼠精子畸形率高于3.8%(P＜0.05).结论在600 mg*kg-1范围内,Fe3O4-CA对小鼠体细胞无致突变性,而对小鼠雄性生殖细胞可能有致突变性.     

营养素对血清中丙二醛含量及人和小鼠精子质量的影响

目的 观察营养素对男性不育患者精子质量,小鼠精子畸形率和血清及精浆中丙二醛(MDA)含量的影响.方法 选择男性不育患者53例,按照WHO精液检验方法进行精液常规检验.按照毒理学精子致畸试验方法对小鼠进行精子致畸影响的研究,采用硫代巴比妥酸比色法测定血清和精浆中MDA含量.本实验的分组为服用营养素前后自身对照.结果 服用营养素后患者精子密度和精液活力明显高于服用前(P<0.05),精子畸形率明显下降(P＜0.01).精子活率参数高于服用前,但统计学差异无统计学意义(P>0.05).小鼠营养素3个剂量组的精子畸形率随着剂量的加大精子畸形率有下降趋势,与阴性对照组比较差异无统计学意义(P>0.05),与阳性对照组比较差异有统计学意义(P<0.05).服用营养素前后血清和精浆中MDA含量差异有统计学意义(P＜0.01).结论 营养素可提高男性不育患者的精子密度,精子活力,降低精子畸形率,并使血清和清浆中MDA含量下降.     

不同剂量137Csγ-射线辐射后造血干/祖细胞辐射敏感性差异研究

摘要：目的 探讨不同剂量137Csγ-射线照射后不同时间点C57 BL/6小鼠造血细胞放射敏感性的差异。方法 选取6~8周龄雄性C57BL/6小鼠72只,完全随机法分为对照组和照射组。照射组小鼠分别接受2、4、6 Gy137Csγ射线一次性全身照射,对照组小鼠接受假照射。小鼠分别于受照后14 d、35d和56d断颈处死,取外周血进行血象测定,取骨髓细胞测定有核细胞数目和造血干/祖细胞数目。结果 不同剂量照射后小鼠的外周血常规指标有明显变化,白细胞数目明显下降,其次是血小板数目,且具有剂量效应关系;在照射后14d,2Gy、4Gy和6Gy照射组小鼠骨髓有核细胞数目与对照组比较分别下降21.9%、39.9%和54.4%（t=4.311、6.401、8.007,P<0.05）;照射后35d和56d,6Gy照射组小鼠骨髓有核细胞和造血祖细胞数目显著低于对照组（t=4.185、3.596,P<0.05）。照射后14d、35d和56d,2Gy、4Gy和6Gy照射组小鼠骨髓造血干细胞数目持续低于对照组（t=9.706、3.427~7.465,P<0.05）。结论 不同剂量137Csγ-射线照射对小鼠造血系统造成不同程度的损伤,造血祖细胞较造血干细胞辐射敏感,且辐射对造血干细胞造成的损伤是持久性的。     

迷迭香酸对γ射线致小鼠骨髓嗜多染红细胞微核的保护作用

目的研究迷迭香酸对γ射线致小鼠骨髓嗜多染红细胞微核的保护作用。方法以骨髓嗜多染红细胞微核形成率为观测指标,C57BL/6J小鼠经60Coγ射线1～3 Gy照射24 h后观察骨髓嗜多染红细胞微核发生率的变化以选择合适的照射剂量;C57BL/6J小鼠经60Coγ射线2Gy照射后不同时间观察骨髓嗜多染红细胞微核发生率的变化以选择照射后取骨髓的时间;2 Gy照射前经迷迭香酸处理的C57BL/6J小鼠照后24 h观察骨髓嗜多染红细胞微核发生率的变化,以确定迷迭香酸对小鼠微核保护作用的剂量效应与时间效应。结果 2 Gy照射24 h后小鼠骨髓嗜多染红细胞微核发生率增加比较明显,适合作为小剂量照射条件;照射后24 h或48 h骨髓嗜多染红细胞微核发生率增加比其他时间明显;经迷迭香酸100 mg/kg连续7次处理后的受照射小鼠骨髓细胞中,微核发生率（6.50‰）明显低于单纯照射组（23.65‰）。结论迷迭香酸对γ射线致骨髓嗜多染红细胞微核具有保护作用。     

五指毛桃水提液对60Coγ射线致小鼠骨髓细胞DNA损伤的防护作用

目的 探讨五指毛桃水提液对60Coγ射线所致的小鼠骨髓细胞DNA损伤的防护作用.方法 40只SPF级♂小鼠随机分为5组:阴性对照组给予生理盐水,辐射模型组单纯接受照射,3个五指毛桃剂量组分别给予相当于生药5,10,20 g.kg-1.d-1五指毛桃水提液,连续灌胃7d.除阴性对照组外,所有小鼠接受全身一次性60Coγ射...     

The investigation of the genotoxic effects of fenarimol and propamocarb in mouse bone marrow in vivo

In this study, we aimed to evaluate the genotoxic effects of fungicides fenarimol and propamocarb which are used to protect crops from fungi. For this reason, bone-marrow micronucleus and chromosome aberration tests were carried out in Swiss albino mice. Mice were injected with four different doses of fenarimol and propamocarb intraperitoneally; 50, 100, 200 and 400 mg/kg b.w. Fenarimol did not induce any significant increase in micronucleated erythrocytes after 24, 36, and 48 h treatment but it decreased the ratio of polychromatic/normochromatic erythrocytes at all dose groups and sampling intervals. Fenarimol did not increase the number of chromosome aberrations significantly, but it reduced the mitotic index at the higher doses (P < 0.05). Propamocarb did not increase the frequency of micronucleated erythrocytes, but decreased the polychromatic/normochromatic erythrocytes ratio at all sampling intervals. Propamocarb increased only gaps in total chromosome aberrations, but when gaps were excluded, there were no significant differences in total aberrations between the control and dose groups (P > 0.05). Propamocarb also reduced the mitotic index compared with the negative control group (P < 0.001). Contributing these results, we can suggest that fenarimol and propamocarb are non-genotoxic in mouse bone marrow in vivo but have cytotoxic effects.     

Lack of effect of coumarin on the formation of micronuclei in an in vivo mouse micronucleus assay.

Coumarin was tested for its potential to cause genotoxic effects in mouse bone marrow cells using an in vivo micronucleus assay. Male and female Swiss mice were administered a single oral dose of coumarin at 50, 100 or 200 mg/kg by gavage in corn oil vehicle. Control animals received only the vehicle. Groups of male mice were also administered mitomycin C at 0.75 mg/kg and served as positive controls. At 24 h after treatment, mice from all dose levels, and at 48 h after treatment, mice from the high dose level only were sacrificed. Bone marrow cells were collected and assayed for the presence of micronuclei. Coumarin did not cause any increase in the incidence of micronucleated polychromatic erythrocytes in male or female mice at any of the dose levels, the positive control mitomycin C produced a significant increase. There was no evidence of coumarin or mitomycin C treatment related cytotoxicity to bone marrow cells. The results of this study demonstrate that coumarin is negative in the mouse in vivo micronucleus assay.     

唐古特大黄多糖组分1对电离辐射损伤小鼠造血系统的影响

目的:探讨唐古特大黄多糖组分1(RTP1)对电离辐射损伤小鼠造血功能的影响。方法:采用雄性6周龄昆明种小鼠,随机分为5组:正常对照组(Normal Control,NC)、辐射对照组(Irradia-tion Control,IC)以及RTP1低剂量组(200mg/kg)、中剂量组(400mg/kg)和高剂量组(800mg/kg),采用灌胃给药方式,连续14d,NC组和IC组则给予等量的生理盐水,第14d除NC组外,各组小鼠均接受6.5Gy/只60Coγ射线照射1次,照射后继续灌胃给药,观察照射后30d小鼠生存情况,并对小鼠骨髓有核细胞数(bonemarrow cell,BMC)、骨髓DNA含量、内源性脾集落形成单位(spleen colony forming unit,CFU-S)及外周血中白细胞(white blood cell,WBC)计数进行检测。结果:与IC组比较,RTP1可提高小鼠30d存活率,并剂量依赖性地升高外周血中WBC计数、骨髓有核细胞数、DNA含量以及脾结节数。结论:RTP1对辐射小鼠的造血系统起到一定保护作用。     

The mutagenic potential of the furylethylene derivative 2-furyl-1-nitroethene in the mouse bone marrow micronucleus test.

The compound 2-furyl-1-nitroethene (G-0) has been tested to determine its ability to induce clastogenic or aneugenic effects in vivo, through the induction of micronucleated polychromatic erythrocytes (MNPCE) in mouse bone marrow. Groups of five CD-1 male mice were administered once intraperitoneally at a dose range of 5-20 mg/kg and bone marrow was sampled at 24 and 48 h after the treatment. G-0 was dissolved in corn oil, thus a vehicle control group received only corn oil at 10 ml/kg. The positive control group was administered with cyclophosphamide (40 mg/kg). All animals dosed with the highest concentration of the test agent (20 mg/kg) showed evident clinical symptoms of toxicity. Although evidences of bone marrow toxicity were observed, no statistically significant increases in the incidence of MNPCE over the vehicle control group were observed at any sampling time with any of the assayed doses of the G-0 compound. Cyclophosphamide treatment increased the incidence of MNPCE in all treated animals, demonstrating the sensitivity of the assay conditions in which it was carried out. From the results obtained, it is concluded that the test agent G-0 is neither clastogenic nor aneugenic in the erythrocytes from the bone marrow of treated mice at the doses tested.     

Evaluation of tissue disposition, myelopoietic, and immunologic responses in mice after long-term exposure to nickel sulfate in the drinking water

Female B6C3F1 mice were exposed to graded doses of nickel sulfate to determine a threshold response for myelotoxicity and immunotoxicity, and to identify which of the populations of lymphoreticular cells were most sensitive to the toxic effects of nickel. Animals were given free access to the chemical in the drinking water at 0, 1, 5, or 10 g/l for 180 d. Water consumption, blood and tissue nickel concentrations, body and organ weights, histopathology, immune responses, bone marrow cellularity and proliferation, and cellular enzyme activities were evaluated. There was no mortality. Mice in the 5-g/l and 10-g/l dose groups drank less water than controls; the responses measured in the 10-g/l group may have been due to a combination of dehydration and chemical toxicity. Decreases in body and organ weights were confined to mice in the 10-g/l dose group, except for the dose-related reductions in thymus weights. Blood nickel was measured at 4, 8, 16, and 23 wk of exposure. The mean blood nickel values showed increases between 4 and 8 wk that were proportional to time and dose; thereafter there was no substantial increase in blood nickel in any of the dose groups, except for an increase in the mean blood concentration in the 10-g/l group at 23 wk. The kidney was the major organ of nickel accumulation. The primary toxic effects of nickel sulfate were expressed in the myeloid system. There were dose-related decreases in bone marrow cellularity, and in granulocyte-macrophage and pluripotent stem-cell proliferative responses. In unfractionated bone marrow cells glucose-6-phosphate dehydrogenase enzyme activity from the hexose monophosphate shunt was more sensitive to nickel sulfate than were representative glycolytic or Krebs cycle enzymes, with 25-35% maximum inhibition at 5 g/l and 10 g/l. Aliquots of bone marrow cells were separated into enriched bands of lymphocytes, granulocyte-macrophages, and erythrocytes; enzyme inhibition that occurred in unfractionated bone marrow cell aliquots was only expressed after cell separation in the enriched granulocyte-macrophage cell population, suggesting that these committed stem cells were a primary target of nickel sulfate toxicity. There was one example of systemic immunotoxicity, reduction in the lymphoproliferative response to lipopolysaccharide, and it was regarded as secondary to the primary effect of nickel sulfate on the myeloid system, since this was the only significant change among a panel of seven immune parameters that were evaluated.     

Cytological effects of khat (Catha edulis) in somatic and male germ cells of mice

Cytological effects of khat (Catha edulis), a popular drug of abuse from Southern Arabia and Eastern Africa, have been studied in Swiss albino mice. The studies on the somatic system involved the use of micronucleus test and the cytological analysis of the mitotic index in the femoral cells of mice. In the micronucleus test, the mice were treated with different doses of khat extract (125, 250 and 500 mg/kg, p.o.) 30 and 6 hours before sacrificing the animals. The polychromatic erythrocytes were screened for the induction of micronuclei. For the analysis of bone marrow cytotoxicity, the mice were treated with the dose of 125, 250 and 500 mg/kg, body weight, p.o. daily for 5 consecutive days. The animals were sacrificed and the femoral cells were microscopically examined for the mitoses. Following the same schedule of treatment, studies on the cytogenetic analysis of meiotic chromosomal aberrations and the sperm head abnormality were undertaken. Khat extract significantly increased the frequency of micronucleated polychromatic erythrocytes, induced bone marrow depression and reduced the mitotic index of the somatic cells. It induced significant chromosomal aberrations viz., aneuploids, autosomal univalents, univalents of the sex chromosomes and polyploids. The frequency of abnormal sperms was also increased.