尾矿库渗漏水污染对泥鳅的氧化损伤作用

【目的】探讨尾矿库渗漏水污染胁迫对泥鳅生理指标的影响,为低浓度环境混合污染的治理提供参考依据。【方法】依据毒理学方法,分别配置不同浓度梯度的尾矿库渗漏水,测定胁迫96 h内泥鳅肾脏、肝脏组织中丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性和谷胱甘肽过氧化物酶（GSH-PX）活性的变化。【结果】尾矿库渗漏水胁迫下,不同浓度处理泥鳅的肝脏和肾脏组织中MDA含量明显高于对照组（P<0.05,下同）,MDA含量与渗漏水处理时间及浓度存在一定的时间—剂量—效应关系。肾脏组织中SOD和GSH-PX活性随渗漏水浓度增加呈先下降后上升的变化趋势;随渗漏水浓度的增加,肝脏组织中SOD活性呈下降趋势,GSH-PX活性变化不显著;肝脏和肾脏组织中的SOD和GSH-PX随胁迫时间延长均无显著的变化规律。【结论】尾矿库渗漏水污染对泥鳅的生理过程有明显抑制作用,且存在毒害效应。     

尾矿库渗漏水污染对泥鳅的氧化损伤作用

【目的】探讨尾矿库渗漏水污染胁迫对泥鳅生理指标的影响,为低浓度环境混合污染的治理提供参考依据。【方法】依据毒理学方法,分别配置不同浓度梯度的尾矿库渗漏水,测定胁迫96h内泥鳅肾脏、肝脏组织中丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性和谷胱甘肽过氧化物酶（GSH-PX）活性的变化。【结果】尾矿库渗漏水胁迫下,不同浓度处理泥鳅的肝脏和肾脏组织中MDA含量明显高于对照组（P〈0．05,下同）,MDA含量与渗漏水处理时间及浓度存在一定的时间一剂量一效应关系。肾脏组织中SOD和GSH-PX活性随渗漏水浓度增加呈先下降后上升的变化趋势;随渗漏水浓度的增加,肝脏组织中SOD活性呈下降趋势,GSH-PX活性变化不显著;肝脏和肾脏组织中的SOD和GSH-PX随胁迫时间延长均无显著的变化规律。【结论】尾矿库渗漏水污染对泥鳅的生理过程有明显抑制作用,且存在毒害效应。     

稀土尾矿库渗漏水污染对花背蟾蜍胚后发育的毒性作用

[目的]明确稀土尾矿库渗漏水污染对花背蟾蜍(Strauchbufo raddei)胚后发育的毒性作用,为稀土尾矿区两栖类动物的保护提供科学依据.[方法]以内蒙古某尾矿库南侧由渗漏水形成的受污染水域湿地(简称尾矿库湿地)为研究样地、相对未受污染的黄河自然保护区小白河湿地(简称小白河湿地)为对照样地,通过观测分析花背蟾蜍的野外生态学指标、生理生化指标和遗传毒性指标,探究稀土尾矿库渗漏水对花背蟾蜍胚后发育的毒性效应.[结果]尾矿库湿地花背蟾蜍的总数、种群密度、性别比例和抱对率均明显少于小白河湿地花背蟾蜍,但产卵量极显著高于小白河湿地(P<0.01,下同);尾矿库湿地的蝌蚪发育相对滞后于小白河湿地蝌蚪,但其体格整体上大于小白河湿地蝌蚪.尾矿库湿地蝌蚪肝胰脏中的总抗氧化能力(T-AOC)呈先下降再上升的变化趋势,于III期达最小值;而丙二醛(MDA)含量的变化趋势恰好相反,于III期达最大值.尾矿库湿地各发育期蝌蚪血细胞DNA损伤程度均极显著高于小白河湿地蝌蚪,且血红细胞核异常率明显高于小白河湿地蝌蚪.[结论]尾矿库渗漏水污染通过影响花背蟾蜍的抱对率来降低蝌蚪种群密度,而对其胚后发育的主要影响机理是导致蝌蚪的组织氧化损伤和血细胞DNA损伤.     

稀土元素铈对镉致泥鳅肝脏DNA损伤的影响

[目的]为稀土元素的研究与应用提供科学依据。[方法]研究稀土元素铈对镉导致的泥鳅肝脏DNA损伤情况的影响。[结果]镉对泥鳅肝脏DNA具有较强的损伤作用,其损伤程度随镉浓度的增加和时间的延长而加重。低、中浓度镉处理组中,断裂的DNA片段较大,最小片段为400 bp左右。高浓度镉处理组中,DNA损伤较严重,200 bp片段较多。加铈后,中、低浓度铈处理组基本未出现DNA Lad-der,说明铈起了缓解作用;高浓度铈处理组出现明显DNA Ladder,片段大小和亮度比高浓度镉单一胁迫组更为明显,说明铈与镉协同对泥鳅DNA产生危害。[结论]低浓度的铈对镉造成的DNA损伤具有缓解作用,高浓度的铈对镉造成强的DNA损伤具有协同作用。     

敌草快对斑马鱼组织损伤及慢性肝脏损害作用

探讨敌草快对斑马鱼(Brachydanio rerio)的毒性效应及其致毒机理。观察敌草快对斑马鱼鳃和肝脏组织的急性损伤效应,并分析慢性敌草快胁迫对斑马鱼肝脏超氧化物歧化酶(SOD)、谷胱甘肽-S转移酶(GST)、丙二醛(MDA)和甘油三酯(TG)的影响。敌草快对斑马鱼的96 h半致死浓度(LC50)为16.92 mg·L~(-1);斑马鱼暴露于8.46、4.23、1.69 mg·L~(-1)敌草快中96 h后,苏木精-伊红(H-E)染色显示鳃小片出现卷曲变形、上皮细胞排列不规则和细胞脱落现象,肝细胞呈现明显的肿大,胞质产生空泡化,局部区域细胞坏死、溶解,斑马鱼鳃和肝脏组织的损伤程度随着敌草快浓度的增加而加重;暴露于1.69、0.84 mg·L~(-1)和0.34 mg·L~(-1)敌草快中28 d后,斑马鱼肝脏的SOD活性变化表现为降-升-降,并呈现出剂量效应;1.69 mg·L~(-1)和0.84 mg·L~(-1)敌草快处理组肝脏的GST活性表现为先升后降,28 d时显著低于对照组(P0.01),0.34 mg·L~(-1)敌草快处理组肝脏的GST活性无显著变化(P0.05);与对照组相比,处理组肝脏的MDA含量在第7 d和14 d变化均不明显(P0.05),在第28 d时0.84 mg·L~(-1)和1.69 mg·L~(-1)敌草快处理组肝脏的MDA含量极显著升高(P0.01);处理组斑马鱼肝脏中TG的含量均从14 d开始出现增加。水体中的敌草快对斑马鱼有较严重的急性损伤作用,长时间暴露于低浓度敌草快中的斑马鱼,其肝脏会发生氧化应激反应,肝脏代谢功能也会受到影响。     

菲、芘对蚕豆的氧化胁迫和DNA损伤

以菲和芘为多环芳烃(PAHs)的代表物,以超氧化物歧化酶(SOD)、过氧化物酶(POD)、过氧化氢酶(CAT)活性和丙二醛(MDA)含量为指标,研究了菲、芘对蚕豆的氧化胁迫;利用彗星实验分析了菲、芘对蚕豆DNA的损伤效应;将蚕豆幼苗根经抗氧化剂维生素E预处理后,暴露于菲、芘污染,研究了DNA损伤与氧化胁迫间的关系。结果表明,供试条件下菲、芘污染导致蚕豆幼苗SOD、POD、CAT活性提高和MDA含量上升,且MDA含量与菲、芘浓度均显著正相关;蚕豆根尖细胞DNA损伤随菲、芘暴露浓度的升高而增大,0~50 mg·kg-1菲污染条件下彗星图像尾矩(TM)值从46.41μm(阴性对照)增加到122.04μm(50 mg·kg-1菲污染处理),增大了162.96%。50mg·kg-1芘暴露下TM值从阴性对照的44.30μm增至110.36μm,增大了149.21%。经抗氧化剂维生素E预处理,蚕豆的DNA损伤程度减小。综上可知,菲、芘对蚕豆产生氧化胁迫并造成根尖细胞DNA损伤,菲、芘诱导的DNA损伤与氧化胁迫有关。     

二甲苯对锦鲤肝脏丙二醛含量和总抗氧化能力的影响

采用暴露试验方法,研究不同浓度的二甲苯在不同暴露时间内对锦鲤肝脏丙二醛(MDA)含量和总抗氧化能力(T-AOC)的影响.结果表明,锦鲤暴露于不同浓度的二甲苯时,其肝脏MDA含量所受的影响较为明显,二甲苯浓度越高,机体产生脂质过氧化的程度越高,对机体造成的氧化损伤越强,试验后期,随着二甲苯暴露浓度的降低,MDA含量呈现逐渐下降的趋势;暴露后20d,高浓度组锦鲤肝脏组织中MDA含量显著增加,表明二甲苯中毒已引起机体发生脂质过氧化,产生氧化损伤;2.24、0.56 mg/L二甲苯在暴露前期能够刺激鱼体肝脏组织T-AOC的增加,4.48 mg/L在暴露期间T-AOC活性呈现出先上升后下降的变化规律,8.96 mg/L二甲苯对锦鲤肝脏T-AOC影响主要以抑制作用为主.在本次暴露试验中,鱼体肝脏MDA和T-AOC对二甲苯污染胁迫的反应较敏感,可将其作为水环境中二甲苯污染的敏感生物标志物.     

单细胞凝胶电泳技术检测蜘蛛血细胞DNA损伤研究

以体外染毒法对星豹蛛雌、雄成蛛进行过氧化氢和甲醛染毒处理,采用单细胞凝胶电泳技术检测蜘蛛血细胞DNA损伤效应,用CASP软件分析彗星图像,并计算受损伤细胞率、彗星尾长和Olive尾矩.结果表明,不同浓度的过氧化氢能引起蜘蛛血细胞DNA断裂损伤,且损伤程度与浓度之间有明显的剂量-效应关系;不同浓度的甲醛能引起蜘蛛血细胞DNA损伤,其中在10ümol/L时引起DNA断裂,在25ümol/L、40ümol/L、55 ümol/L时引起DNA交联,而在70ümol/L时引起血细胞凋亡.     

Cr6+污染致大麦幼苗基因组DNA损伤效应的研究

应用随机扩增DNA多态性(RAPD)技术,研究了Cr6 胁迫对大麦幼苗DNA含量的影响及根系基因组DNA的损伤效应.结果表明,在5～80 mg·L-1的Cr6 浓度范围内处理7 d后,大麦幼苗根系的DNA含量随Cr6 处理浓度的增加明显降低,各处理组的DNA含量均低于对照,其中,5～40mg·L-1Cr6 处理组的DNA含量降幅最大.Cr6 处理后大麦幼苗根系的DNA增色效应随浓度升高呈现先增后减的趋势,5～20 mg·L-1的Cr6 浓度范围内大麦DNA的增色效应明显高于对照,其中10 mg·L-1Cr6 的DNA增色效应最为显著,而40 mg·L-1以上的Cr6 外理后增色效应下降.Cr6 胁迫使大麦基因组的RAPD图谱发生变化,包括DNA谱带的增加、减少及其荧光强度的改变,且DNA多态性谱带的变化与Cr6 浓度具有正相关效应.通过对大麦基因组的DNA损伤的检测.可以评估Cr6 污染对植物的遗传毒害效应.     

苏丹红I对泥鳅红细胞微核率和组织磷酸酶活性的影响

[目的]为明确苏丹红Ⅰ的危害提供试验依据。[方法]用不同浓度(0.312 5、0.625、1.25、2.50和5.00 mg/L)苏丹红Ⅰ处理泥鳅后8、162、4、32和40 h,观察带有微核的红细胞数,并测定肝脏、肌肉和肾脏组织中磷酸酶活性,研究苏丹红Ⅰ对泥鳅红细胞微核率和不同组织中磷酸酶活性的影响。[结果]泥鳅红细胞微核的自然发生率为1.128 3‰。经不同浓度苏丹红处理一定的时间后,泥鳅红细胞微核率较对照组均显著提高,最高达6.063 6‰。随着苏丹红Ⅰ浓度的提高,泥鳅红细胞微核率出现最高峰的时间也相应提前。染毒后各组织的酸性磷酸酶(ACP)活性迅速上升,而碱性磷酸酶(ALP)活性迅速下降。[结论]泥鳅红细胞微核率与苏丹红Ⅰ浓度大体上呈正相关,同时也有一定的时间效应。     

LSD and genetic damage

Of nine studies in vitro, six have indicated some degree of induced chromosomal breakage after exposure to LSD; three failed to confirm these results. The damage, when found, was generally of the chromatid type, arising during or after DNA synthesis. This damage, with one exception, was the result of concentrations of drug and durations of exposure which could not be achieved in humans with reasonable dosages. There did not appear to be a dose-response relation. The magnitude of damage, when found, was in the range encompassing the effects of many commonly used substances. The absence in vitro of excretory and detoxifying systems present in vivo, as well as several negative reports, cast doubt on the relevance of in vitro results. In 21 chromosomal studies in vivo, 310 subjects were examined. Of these, 126 were treated with pure LSD; the other 184 were exposed to illicit, "alleged" LSD. A maximum of only 18 of 126 (14.29 percent) of the subjects in the group exposed to pure LSD showed higher frequency of chromosome aberration than the controls. In contrast, a maximum of 90 of 184 (48.91 percent) of the subjects taking illicit LSD showed an increase in frequency of aberrations. Of all the subjects reported to have chromosome damage, only 18 of the 108 (16.67 percent) were exposed to pure LSD. The frequency of individuals with chromosomal damage reported among illicit drug users was more than triple that associated with the use of pharmacologically pure LSD. We conclude that chromosome damage, when found, was related to the effects of drug abuse in general and not, as initially reported, to LSD alone. We believe that pure LSD ingested in moderate dosages does not produce chromosome damage detectable by available methods. No significant work on carcinogenic potential of LSD has been reported so far. No cause-and-effect relation and no increase in the incidence of neoplasia among LSD users have been demonstrated. Case reports (three in 4.0 years) of leukemia and other neoplasia in this population are rare. The results of early chromosome studies suggested that true genetic damage might be a consequence of LSD exposure. The comprehensive evidence from studies on drosophila indicates no mutagenic effect from 0.28 to 500 microg of LSD per milliliter and a definite mutagenic effect from 2,000 to 10,000 microg/ml; this is consistent with a threshold response or a sigmoid dose-effect relation. We believe that LSD is, in fact, a weak mutagen, effective only in extremely high doses; it is unlikely to be mutagenic in any concentration used by human subjects. Circular dichroism experiments suggested that the specific mechanism of action of LSD on DNA may be a direct interaction resulting in conformational changes in the DNA helix. These changes are unlikely to result in a decrease of internal stability sufficient to cause breakage of chromosomes, but they may be the physical basis of the weak mutagenicity. Early chromosomal studies implicated LSD as a potential cause of congenital malformations, fetal wastage, and germinal chromosome damage. First reports of a teratogenic effect in hamsters and rats have not been confirmed. A review of 15 rodent studies indicated a wide range of individual, strain, and species susceptibility to the effects of LSD. The applicability of such investigations to man is doubtful. In a study of human pregnancies, those exposed to illicit LSD had an elevated rate of spontaneous abortions. There is no reported instance of a malformed child born to a woman who ingested pure LSD; there are six cases of malformation associated with exposure to illicit LSD, four of which have similar limb defects. Given, however, the high frequency of unexplained "spontaneous" birth defects, the rare occurrence of malformed infants born to women who used illicit LSD may be coincidental. While there is no evidence that pure LSD is teratogenic in man, the use of any drug during pregnancy requires that its potential benefits significantly outweigh its potential hazards. From our own work and from a review of the literature, we believe that pure LSD ingested in moderate doses does not damage chromosomes in vivo, does not cause detectable genetic damage, and is not a teratogen or a carcinogen in man. Within these bounds, therefore, we suggest that, other than during pregnancy, there is no present contraindication to the continued controlled experimental use of pure LSD. Note added in proof: A brief review has been brought to our attention. Although based on a sample of only 15 studies the author reached conclusions similar to our own (92).