毒死蜱对子代雄鼠性激素相关基因mRNA表达的影响

有机磷类农药毒死蜱 (chlorpyrifos，CPF) 可影响雄性动物生殖系统功能。为探究胚胎早期毒死蜱暴露对雄性小鼠生殖功能的影响，于母鼠妊娠后第7天 (gestational day, GD7) 至分娩前1 d每天给予母鼠灌胃染毒10 mg/kg (b.w.) 剂量的毒死蜱，于子代雄鼠出生后第42 天处死，取血液及睾丸，测定睾丸质量，通过酶联免疫法检测血液中睾酮 (testosterone，T) 及促黄体生成素 (luteinizing hormone，LH) 含量，同时采用RT-qPCR方法检测睾丸中与胆固醇及睾酮合成相关的5个基因mRNA表达的变化。结果显示:与对照组相比，毒死蜱染毒组子代鼠睾丸质量增加了16.5%，差异极显著 (P < 0.01)；血清中睾酮及促黄体生成素含量分别增加了9.9%和6.2%，但与对照差异不显著 (P > 0.05)。睾丸中胆固醇合成基因HMG-CoA synthase的mRNA表达量升高了72.9%，运输基因StAR的mRNA表达量升高了45.3%；此外，睾丸中睾酮合成基因P450scc、P450-17α和3β-HSD的mRNA表达量分别升高了95.5%、68.9%和112.0%。各基因mRNA的表达量在染毒组与对照组间均差异极显著 (P < 0.01)。研究表明，毒死蜱暴露可影响子代雄鼠睾酮合成相关基因mRNA的表达，推测毒死蜱可能是通过该途径发挥其毒性作用。     

乙烯利对昆明种小鼠的氧化应激作用

选用小鼠血清及脾脏组织中超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活力及丙二醛(MDA)含量为观察指标,从机体氧化和抗氧化系统是否失衡的角度研究了乙烯利的氧化应激作用。结果表明,乙烯利能明显降低小鼠血清及脾脏组织中SOD和GSH-Px的活性。其中:134,268 mg/kg bw剂量处理组血清SOD和GSH-Px活性分别降低了8.91% ,12.44%和4.18% ,8.54% ;268, 536 mg/kg bw剂量组脾脏SOD和GSH-Px活性分别降低了8.34% ,19.61%和9.72%,24.86% ;与对照组差异显著(PP<0.01)。结果显示,乙烯利能破坏小鼠机体氧化和抗氧化系统的平衡,引起氧化应激。     

杀虫安对小鼠脑组织内神经递质的影响

研究了杀虫安经灌胃给药后对小鼠脑组织内多巴胺及氨基酸含量的影响。将60只ICR (美国癌症研究所)小鼠随机分为空白对照、杀虫安低剂量(200 mg/kg bw)及高剂量(300 mg/kg bw) 3个处理组,于灌胃后出现惊厥时断头取脑,采用高效液相色谱-电化学(HPLC-ECD)检测法测定了鼠脑组织内多巴胺(DA)及其代谢产物二羟苯乙酸(DOPAC)和高香草酸(HVA)的含量,采用液相色谱-质谱联用(LC-MS/MS)法测定了氨基酸的含量。结果发现,两个剂量处理组鼠脑组织内DA及氨基酸含量与对照相比均有显著性差异。其中:DA比对照分别升高25.25%和31.93%(PPPPγ-氨基丁酸(GABA)含量比对照降低32.55% (PP<0.05)。表明杀虫安导致惊厥时伴有鼠脑内多巴胺和氨基酸含量的变化。     

Β-蜕皮激素对异色瓢虫羧酸酯酶基因表达及酶活性影响的初步研究

为了探明β-蜕皮激素对异色瓢虫的作用及其安全剂量,本研究利用实时定量PCR(RT-PCR)和比色法测定了异色瓢虫3龄幼虫施用不同浓度的β-蜕皮激素体内羧酸酯酶活性与基因表达情况.结果表明:用0.1、0.5、1 mg/L β-蜕皮激素处理异色瓢虫3龄幼虫,在处理后4～48 h内CarE mRNA水平和CarE比活力呈现先升高、保持正常水平或略下降、再升高、然后很快恢复正常的规律.到处理后的第48 h,处理组的CarE mRNA表达量和CarE比活力均恢复到正常水平.所以,认为在低于1 mg/L浓度下应用β-蜕皮激素控制害虫对异色瓢虫的3龄幼虫安全.而利用5 mg/L或10 mg/L的β-蜕皮激素处理异色瓢虫3龄幼虫,CarE mRNA表达量和CarE比活力均表现出长期的被抑制效应,特别是到处理24 h后,CarE mRNA表达量和CarE活性不仅未能恢复到正常水平,反而一直处于极低的水平.因此,认为这两个浓度对异色瓢虫3龄幼虫不安全.     

10%溴虫腈悬浮剂对野鸭繁殖性能的影响

试验测定了10%溴虫腈悬浮剂对野鸭(Mallard duck)慢性繁殖的影响。溴虫腈试验浓度(有效成分)分别设计为0(对照)、0.5、1.0、2.0 mg/kg饲料。结果表明:溴虫腈对野鸭蛋产起始时间有一定影响,随着处理剂量的提高,初产蛋的时间略向后移;溴虫腈对野鸭蛋的蛋壳厚度、受精率及孵化率均没有影响;雏鸭14 d的成活率(以孵化出鸭数计),对照组、0.5 mg/kg饲料组、1.0 mg/kg饲料组、2.0 mg/kg饲料组分别为31.6%、29.2%、16.7%和17.0%。     

氯吡脲连续灌胃给药4周对大鼠的毒性作用

为明确氯吡脲对大鼠的毒性作用,采用150、300和600 mg/kg剂量分别向SD大鼠灌胃 (ig) 给予氯吡脲,每日1次,连续给药4周。每日观察大鼠的中毒状况和死亡情况,每周记录体质量和摄食量;于停药后第1天和第15天分别处死SD大鼠,检测血常规、血清生化和凝血功能;取主要脏器进行称量,计算其脏器系数并进行常规病理组织学检查。结果发现:连续给药4周,氯吡脲对大鼠体质量、摄食量、血常规和凝血均无明显影响。停药后第1天,与溶剂对照组比较,氯吡脲300 mg/kg及以上剂量处理组雄性大鼠的尿素氮和肌酐含量明显升高 (P < 0.05),600 mg/kg剂量组血糖显著升高 (P < 0.05),其中,600 mg/kg处理组雄性大鼠的尿素氮、肌酐和血糖分别是对照的1.9、1.6和1.3倍。氯吡脲300 mg/kg及以上剂量组雌、雄性大鼠的肾脏系数均明显升高 (P < 0.05),其中300 mg/kg剂量组雌、雄性大鼠的肾脏系数分别是对照的1.2和1.1倍,600 mg/kg剂量组雌、雄性大鼠的肾脏系数分别是对照的1.4和1.1倍;300 和600 mg/kg剂量组雌性大鼠的肝脏系数明显升高 (P < 0.01),分别是对照的1.3和1.9倍。病理切片检查可见肾脏病理组织学改变,主要表现为轻度肾管萎缩,明显的白细胞管型、透明管型、间质炎性细胞浸润及肾小管扩张。停药后第15天,上述毒性反应症状有所恢复。研究表明,SD大鼠经连续灌胃给予氯吡脲4周,在600 mg/kg剂量下表现为明显肾脏毒性反应,在300 mg/kg剂量下表现为较轻微的肾脏毒性反应,推测氯吡脲的主要毒性靶器官可能是肾脏;其未见明显毒性反应剂量为150 mg/kg。     

鱼藤酮对小鼠脑神经递质多巴胺及其代谢产物的影响

研究了注射鱼藤酮对C57BL/6N小鼠神经递质多巴胺的影响。给小鼠皮下注射鱼藤酮(10 mg/kg)两次,间隔2 h,在第2次注射8 h后分离脑组织样品,并应用高效液相色谱仪配电化学检测器,测定了小鼠脑内多巴胺(DA)及其主要代谢物3,4-二羟苯酰乙酸(DOPAC)和高香草酸(HVA)的水平。结果表明,第2次注射8 h后,鱼藤酮处理组的脑内DA、DOPAC和HVA水平分别比对照组高40.5%、544.4%和168.2%,差异显著(P<0.01)。实验显示,鱼藤酮对多巴胺能神经系统具有毒性作用。     

氯虫苯甲酰胺和氟虫腈对黏虫细胞色素P450基因表达的影响

为筛选出黏虫Mythimna separata参与杀虫剂解毒代谢的主效细胞色素P450基因,采用叶片浸渍法测定了用于处理黏虫3龄幼虫的亚致死浓度,通过构建转录组测序文库并结合数字基因表达(digital gene expression,DGE)对不同处理的黏虫进行测序,并运用实时荧光定量PCR(realtime quantitative polymerase chain reaction,RT-qPCR)技术验证12个P450基因的表达情况。结果表明,用于处理黏虫的氯虫苯甲酰胺和氟虫腈亚致死浓度LC_(10)分别为0.15、13.66 mg/L;对照样品、氟虫腈处理样品和氯虫苯甲酰胺处理样品分别获得59 521 504、64 838 148和41 722 990个原始序列数据,分别获得57 441 216、62 368 912和40 285 164个过滤后的序列数据;过滤后的序列长度分别为8.62、9.36和6.04 G;碱基错误率均为0.02%;Phred数值大于20、30的碱基占总碱基的百分比均高于90.59%;鸟嘌呤+胞嘧啶(guanine cytosine,GC)含量分别为47.16%、48.94%和47.55%,表明转录组测序质量较高;黏虫受氯虫苯甲酰胺胁迫后,29个P450基因表达量上调,27个P450基因表达量下调;黏虫受氟虫腈胁迫后,23个P450基因表达量上调,26个P450基因表达量下调;12个P450基因表达量的RT-qPCR技术检测结果与DGE测序文库显示的结果基本一致。     

吡虫啉微囊种衣剂在小麦田中的剂量动态及对蚜虫防效研究

采用超高效液相色谱—串联质谱测定了吡虫啉微囊悬浮种衣剂在土壤和小麦植株组织内的剂量动态及对拔节期、灌浆期小麦蚜虫的防治效果。试验结果表明,微囊化剂型可以显著延缓吡虫啉在小麦根际土壤中的降解。种子包衣处理相同有效成分用量4 g/kg,小麦播种后175 d,微囊悬浮种衣剂处理区小麦根际土壤与小麦组织内的吡虫啉含量分别为0.80 mg/kg和0.099 mg/kg,均分别显著高于吡虫啉常规剂型处理区(0.21 mg/kg、0.035 mg/kg)。吡虫啉微囊悬浮种衣剂有效成分用量2、4 g/kg种子处理,对小麦拔节期蚜虫(药后175 d)的防效分别为92.46%、95.32%,对小麦灌浆期蚜虫(药后205 d)的防效分别为84.00%、85.07%;相同有效成分用量下,吡虫啉悬浮种衣剂处理区对小麦拔节期蚜虫的防效分别为78.01%、85.01%,对小麦灌浆期蚜虫防效分别为60.10%、65.47%;相同用量下比常规种衣剂对小麦拔节期和灌浆期蚜虫防效分别提高10%和20%。     

不同浓度香豆素水溶液对黑麦草幼苗的影响

在温室条件下,采用土壤盆栽技术研究不同浓度的香豆素水溶液对多花黑麦草(Lolium multiflorum)幼苗生理生化变化的影响。结果表明,在香豆素水溶液浓度分别为0 mg/kg、100 mg/kg、200 mg/kg、500 mg/kg、1 000 mg/kg和2 000mg/kg处理下,多花黑麦草幼苗根基部呈暗黄色且易断,叶尖枯黄;随着浓度的升高,叶片颜色加深,叶基部和叶尖坏死,致死率也逐渐升高;长度、鲜重、干重和叶绿素含量降低,丙二醛(MDA)含量升高,可溶性糖(SS)和脯氨酸(PRO)含量先升高后降低,这表明多花黑麦草对低浓度的香豆素有一定的抵抗能力,但在高浓度的香豆素水溶液处理下则受到伤害。     

Nephrotoxicity in rats induced by organophosphate insecticide methidathion and ameliorating effects of vitamins E and C

The effects of organophosphate insecticide methidathion (MD) on kidney tissue and the ameliorating effects of a combination of vitamins E and C against subchronic MD toxicity were evaluated in rats. Experimental groups were: control group (group I), 5 mg/kg body weight MD-treated group (group II), and 5 mg/kg body weight MD plus vitamin E plus vitamin C treated group (group III). The groups II and III were treated orally with MD on five days a week for four weeks. Vitamins E and C were injected at doses of 50 mg/kg body weight, i.m. and 20 mg/kg body weight, i.p., respectively, 30 min after the treatment of MD in the group III. Rats were anaesthesized and venous blood samples were collected by direct right ventricle heart puncture, in addition, the right kidney was removed for histopathological examinations and malondialdehyde (MDA) analyses after four weeks. The serum activity of cholinesterase (ChE) and the kidney level of malondialdehyde, and kidney histopathology were studied in rats. MD caused decreased ChE activity (group I: 2114 ± 63 U/L, group II: 1455 ± 100 U/L) and increased MDA level (group I: 147 ± 20.2 nmol/mg protein, group II: 236 ± 25.6 nmol/mg protein), and kidney damage in rats. Furthermore, a combination of vitamins E and C restored partially (ChE activity: 1670 ± 111 U/L, MDA level: 159 19.4 nmol/mg protein) this changes in MD-treated rats.     

Neurotoxicity in murine striatal dopaminergic pathways following co-application of permethrin, chlorpyrifos, and MPTP

The neurotoxic action of permethrin and chlorpyrifos on striatal dopaminergic pathways was investigated in C57BL/6 mice. Technical permethrin (50/50 ratio of cis and trans isomers, 200 mg/kg) and/or chlorpyrifos (75 mg/kg) were administered three times over a two-week period, with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 20 mg/kg) given on day one. Alterations in expression of α-synuclein, dopamine transporter (DAT), and tyrosine hydroxylase (TH) were analyzed at 1 or 28 days post-treatment. MPTP alone produced a long-lasting lesion in striatal dopaminergic pathways, with a depression of TH and DAT protein at both post-treatment times. Chlorpyrifos or permethrin alone had no effect on TH or DAT expression levels. No greater effect on protein expression was observed in mice treated with both MPTP and insecticides at 1 day post-treatment. However, by day 28 a significant reduction (p < 0.05) of TH and DAT was observed in the mice treated with MPTP, permethrin, and chlorpyrifos, compared with the mice given MPTP alone. Significant alteration (p < 0.05) of α-synuclein expression by MPTP (45% decrease) and permethrin (20% increase) occurred at 1 day post-treatment, but reverted to control levels by day 28. Parallel experiments with pure cis or trans isomers of permethrin (100 mg/kg), showed that each isomer caused about half the up-regulation of α-synuclein. These findings demonstrate that the co-application of pyrethroid or organophosphorus insecticides enhance the neurotoxicity of MPTP in C57BL/6 mice, and that a slowly developing neurotoxicity may occur after termination of high-dose exposure.     

The effects of organophosphate insecticide diazinon on malondialdehyde levels and myocardial cells in rat heart tissue and protective role of vitamin E

Diazinon is an organophosphate insecticide has been used in agriculture and domestic for several years. Vitamin E (200 mg/kg, twice a week), diazinon (10 mg/kg, per day), and vitamin E (200 mg/kg, twice a week)+diazinon (10 mg/kg, per day) combination was given to rats orally via gavage for 7 weeks. Body and heart weights, malondialdehyde (MDA) level in heart tissue and ultrastructural changes in myocardial cells were investigated at the end of the 1st, 4th, and 7th weeks comparatively with control group. When diazinon-treated group was compared to control group body and heart weights were decreased significantly at the end of the 4th and 7th weeks. It was observed that, at the end of 1st, 4th, and 7th weeks there was a statistically significant increase in MDA levels when diazinon- and vitamin E +diazinon-treated groups were compared to control group. While at the end of the 1st week statistically significant changes were not being observed, at the end of 4th and 7th weeks statistically significant decrease was detected in MDA levels when vitamin E+diazinon-treated group was compared to diazinon-treated group. In our electron microscopic investigations, while vacuolization and swelling of mitochondria myocardial cells of diazinon-treated rats were being observed, swelling of several mitochondria were observed in vitamin E+diazinon-treated rats. We conclude that vitamin E reduces diazinon cardiotoxicity, but vitamin E does not protect completely.     

Selenium and vitamin E, natural antioxidants, protect rat cerebral cortex against dimethoate-induced neurotoxicity

Pesticides have been used in agriculture to enhance food production by eradicating unwanted insects and controlling disease vectors, nevertheless occupational exposure to high levels of these compounds can lead to neurodegenerative disorders, characterized by serious oxidative and neurotoxic effects. However, there is a lack of consensus as to which determinations are best used to quantify future risks arising from xenobiotic exposure and natural antioxidant interventions. Our study aims to determine the potential ability of selenium and/or vitamin E, used as nutritional supplements, to alleviate oxidative stress in cerebral cortex tissue induced by dimethoate, an organophosphorus pesticide. Adult Wistar rats were exposed either to dimethoate (0.2 g/L of drinking water), dimethoate + selenium (0.5 mg/kg of diet), dimethoate + vitamin E (100 mg/kg of diet), or dimethoate + selenium + vitamin E, for 30 days. Exposure to dimethoate increased malondialdehyde levels, protein carbonyl groups and advanced oxidation protein products, while Na⁺K⁺-ATPase, acetylcholinesterase and butyrylcholinesterase activities decreased in the cerebral cortex. An increase in glutathione peroxidase, superoxide dismutase and catalase activities and a decrease in glutathione, non-protein thiols and vitamin C levels were observed. Administration of selenium and/or vitamin E through the diet in dimethoate treated rats ameliorated the biochemical parameters cited above. The histological findings confirmed the biochemical results. The model of this study that we employed characterized the relationships between dimethoate-induced neurotoxicity and its alleviation by natural antioxidants like selenium and vitamin E. These elements may be considered beneficial for the protection of cerebral cortex against injury induced by dimethoate.     

Chlorpyrifos-induced oxidative stress and histological changes in retinas and kidney in rats: Protective role of ascorbic acid and alpha tocopherol

This study was undertaken to evaluate the antioxidant effect of vitamins C and E against oxidative stress, apoptosis and histological changes of kidney and retina in CPF-treated rats. Forty male Sprague-Dawley rats were divided into four groups including the control group, the group treated orally with a single dose of CPF (63 mg/kg b.w.), the group injected intramuscularly (i.m.) with vitamin C (250 mg/kg b.w.), and intraperitonealy (i.p.) with vitamin E (150 mg/kg b.w.) daily for 7 days and the group treated with CPF (single dose) and injected with vitamins (for 7 days). The results showed that CPF induced apoptosis and severe oxidative stress as indicated by the significant increase in MDA and sFasL concentration and the significant decrease in GSH concentration in serum. Co-administration of vitamins C and E ameliorate these toxic effects and improved the histological pictures of kidneys and retinas. It could be concluded that combined administration of vitamins C and E is useful in the routine therapy for the protection against tissue damage induced by CPF.     

金丝草抑菌活性成分研究

为探索金丝草Pogonatherum crinitum在植物病原菌防治方面的应用前景,测定了金丝草水提取物及其乙酸乙酯、正丁醇萃取物对20种常见农作物病原真菌的抑菌活性。结果表明,2.00×103 mg/L的乙酸乙酯萃取物对其中8种植物病原菌的抑制率大于50%,尤其对辣椒疫霉Phytophthora capsici的抑制率高达100%。由乙酸乙酯萃取物进一步分离得到10个已知化合物,经波谱学方法鉴定其分别为1,2,4-三羟基苯（ 1 ）、1,2-二羟基-4-甲氧基苯（ 2 ）、小麦黄素-7-O-β-D-吡喃葡萄糖苷（ 3 ）、小麦黄素（ 4 ）、β-腺苷（ 5 ）、咖啡酸（ 6 ）、留兰香木脂素B（ 7 ）、木犀草素6-C-β-波依文糖-7-O-β-葡萄糖（ 8 ）、芦丁（ 9 ）及槲皮素（ 10 ）,其中化合物 2、3、5、7 和 10 为从该植物中首次分离得到。孢子萌发法测定结果表明:化合物 6~10 对棉花立枯丝核菌Rhizoctonia solani和辣椒疫霉的孢子萌发具有较好的抑制作用,其EC₅₀值分别在18.54~103.6 mg/L和21.38~87.83 mg/L之间。     

威百亩熏蒸对土壤硝化作用及amoA型硝化细菌群落结构的影响

为探究威百亩对土壤硝化作用的影响及作用机制,通过理化分析和变性梯度凝胶电泳方法研究浓度为20、100和500 mg/kg威百亩熏蒸处理对土壤硝化作用及amoA型硝化细菌群落结构的影响。结果表明,威百亩熏蒸处理0、14、28 d后,3种浓度处理的土壤硝化率与对照差异不显著;处理56 d后,20、100和500 mg/kg浓度处理的土壤硝化率分别为81.15%、76.66%和94.08%,前两者与对照差异不显著,后者与对照差异显著;而处理84 d后,3种浓度处理的土壤硝化率与对照差异均不显著。与对照相比,3个浓度威百亩熏蒸处理不同时间后土壤amoA型硝化细菌群落的均匀度指数差异不显著。熏蒸处理14 d后,浓度20、100 mg/kg威百亩处理的土壤amoA型硝化细菌群落的香农多样性指数和丰富度指数分别为1.00、10.97和0.84、7.79,与对照的0.92和9.78均无显著差异;而浓度500 mg/kg威百亩处理的香农多样性指数和丰富度指数分别为0.59、5.77,显著低于对照。表明威百亩对土壤硝化强度的影响较amoA型硝化细菌群落延迟,说明土壤中硝化作用的强弱并非完全决定于土壤amoA型硝化细菌的作用。     

Modulation of ethion-induced hepatotoxicity and oxidative stress by vitamin E supplementation in male Wistar rats

Organophosphorus insecticides (OPIs) may induce oxidative stress leading to generation of free radicals and alteration in antioxidant system of animals. Many studies reported that enzymatic and non-enzymatic antioxidant may play protective role against OPIs induced toxicity in human and rats. The aim of present study was to investigate the possible protective role of vitamin E on ethion-induced hepatotoxicity in rats using qualitative, quantitative and biochemical approaches. Adult male albino rats of Wistar strain were randomly divided into four groups; each group consists of six animals. Animals were treated for a period of 28 days. Group I (control group received corn oil); Group II [ethion treated (2.7 mg/kg bw/day)]; Group III (vitamin E treated (50 mg/kg of bw/day)]; Group IV (ethion + vitamin E treated). Animals were sacrificed after 7, 14, 21 and 28 days by decapitation and liver tissue was used for the measurement of proteins, lipid peroxidation (LPO), reduced glutathione (GSH) content and activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) glutathione reductase (GR) and glutathione-S-transferase (GST). Erythrocytes were analyzed for acetyl cholinesterase activity. The result of this study shows that in vivo administration of ethion caused a significant induction of oxidative damage in liver tissue as evidenced by increased level of LPO and decreased GSH content. Ethion toxicity also led to a significant increase in the activities of SOD, CAT, GPx and GST in liver tissue. In addition, decrease in GR activity was observed in ethion administered rats compared to control. Histopathological findings revealed that exposure to ethion caused damage in liver tissue. However, simultaneous supplementation with vitamin E restored these parameters partially. In conclusion, the results of the current study revealed that ethion-induced toxicity caused lipid peroxidation, alterations in the antioxidant enzymes and histopathological changes in liver. Supplementation of vitamin E exhibited protective effect by inhibiting ethion-induced toxicity in liver and erythrocytes.     

Biphenyl hydroxylation and its induction differ between montane voles and Swiss Webster mice

Hepatic microsomes from female montane voles, Microtus montanus, metabolized biphenyl to 4-hydroxybiphenyl (359 ng/mg microsomal protein/min), 3-hydroxybiphenyl (49 ng/mg/min), and 2-hydroxybiphenyl (29 ng/mg/min). Phenobarbital treatment of the voles (ip) induced in vitro biphenyl hydroxylations by about 324, 865, and 445% for 4-, 3- and 2-hydroxylation, respectively. Comparable studies were made of female, white Swiss Webster mice. The major microsomal metabolite was 4-hydroxybiphenyl (1010 ng/mg/min) but more 2-hydroxybiphenyl (118 ng/mg/min) was formed than 3-hydroxybiphenyl (92 ng/mg/min). Phenobarbital treatment of the mice barely changed biphenyl 2-hydroxylation (?1.3%) but did raise 3- and 4-hydroxylation (55 and 211%, respectively). Treatment of voles with 3-methylcholanthrene raised biphenyl 2-, 3-, and 4-hydroxylation by about 81, 50, and 47%, respectively, whereas in mice the increases were 176, 41, and 31%, respectively. β-Naphthoflavone treatment had similar effects. The vole liver microsomes were dependent upon NADPH for biphenyl hydroxylation. The carbon monoxide difference spectra of reduced cytochrome in the microsomes show a peak at 450.4 nm. This was unchanged by phenobarbital and only slightly shifted (?0.8 nm) by 3-methylcholanthrene or β-naphthoflavone treatment. Voles and mice represent different families of the order Rodentia. The results obtained with voles more closely resemble those reported for hamsters which are in the same family but a different subfamily than voles. Comparative consideration of the taxonomic relations of the rodents, therefore, may be useful in interpreting their comparative toxicology.