饲喂不同浓度黄曲霉毒素B1饲料对花鳗鲡幼鱼生长、抗氧化能力和毒素积累的影响

以含不同浓度黄曲霉毒素B₁(AFB₁) (0、10、100和1000 μg/kg饲料)的4种饲料饲喂平均初始体重为(6.41±0.10) g的花鳗鲡(Anguilla marmorata)幼鱼56d, 探讨AFB₁对花鳗鲡幼鱼生长性能、抗氧化能力、肝脏组织结构及鱼体肌肉中的毒素积累的影响。结果表明, 各实验组幼鱼均未表现出行为及体色的异常。1000 μg/kg毒素组幼鱼的存活率、终末体重、摄食率、特定生长率和饲料效率显著低于对照组, 10 μg/kg毒素组和100 μg/kg毒素组与对照组无显著差异。10 μg/kg毒素组幼鱼肝脏超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)、谷胱甘肽S转移酶(GST)活性和丙二醛(MDA)含量与对照组无显著差异。饲料AFB₁含量≥100 μg/kg显著影响花鳗鲡幼鱼肝脏的超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和谷胱甘肽转移酶(GST)活性。对照组和10 μg/kg毒素组幼鱼肝脏组织学观察未发现明显病理变化。1000 μg/kg毒素组幼鱼的肝脏细胞表现出严重的空泡化。随着饲料AFB₁水平的升高, 幼鱼肝脏和肌肉中AFB₁积累量均显著升高。1000 μg/kg毒素组幼鱼肝脏和肌肉中AFB₁积累量分别为17.75和5.98 μg/kg, 均超过FDA食品安全限定标准(5 μg/kg)。由此可见, 饲料中AFB₁≤10 μg/kg对花鳗鲡幼鱼是相对安全的浓度。     

青霉吸附水体重金属铬条件与特性研究

目的:研究青霉(Penicillium lh-1)作为吸附剂去除水体中六价铬的吸附条件与吸附特性.方法:菌种摇瓶培养收获茵体,干燥粉碎分选,添加吸附剂到体积100ml浓度50mg/L六价铬溶液中,对最优吸附温度、pH、共存离子以及铬被吸附形式进行研究.结果:①温度28℃以及酸性环境(pH 3)为最优吸附条件,10 h内,Cr(Ⅵ)的生物吸附去除效率达99%.②铬的生物吸附主要以六价形式,约占80%,部分Cr(Ⅵ)被还原成Cr(Ⅲ),约占20%.③溶液中共存离子对六价铬吸附的影响不同,一价阴离子与Cu2+对Cr(Ⅵ)的吸附几乎没有影响,二价阴离子和Ni2+的存在却明显地影响了生物吸附剂对Cr(Ⅵ)的吸附.结论环境温度、溶液pH以及溶液中共存离子对铬的生物吸附有显著的影响.     

隐藏嗜酸菌Acidiphilium cryptum XTS的Cr(Ⅵ)还原特性及相关基因的差异表达

[目的]考察pH值、初始Cr(Ⅵ)浓度、Fe(Ⅲ)的加入及氧气含量对隐藏嗜酸菌Acidiphiliumcryptum XTS还原Cr(Ⅵ)的影响及其六价铬还原相关基因在不同培养条件下的差异表达.[方法]采用正交试验法L9(34)优选Cr(Ⅵ)还原最适条件;根据模式菌A.cryptum JF-5同源功能基因序列设计引物,对菌株XTS中的六价铬还原相关基因Acry_2099在不同培养条件下的基因差异表达进行分析.[结果]pH为2.9,初始Cr(Ⅵ)浓度为80 mg/L,Fe(Ⅲ)浓度为100 mg/L的条件是该菌株还原Cr(Ⅵ)的最优化配合比,在该条件下处理24 h,Cr(Ⅵ)的还原率达到67.48％;从菌株XTS中成功克隆了Acry 2099基因,其序列与模式菌A.cryptum JF-5的同源功能基因序列一致性达到了99.7％;在不同pH值、初始Cr(Ⅵ)浓度及氧气含量下Acry_2099基因表达上调情况与Cr(Ⅵ)还原速率呈一致趋势,证明Acry 2099很可能参与还原Cr(Ⅵ)的代谢途径.虽然加入Fe(Ⅲ)能促进Cr(Ⅵ)的还原,但是铁的加入对Acry 2099基因表达水平没有显著的影响.[结论]A.cryptumXTS对Cr(Ⅵ)的还原与pH值、初始Cr(Ⅵ)浓度、Fe(Ⅲ)的存在等因素有关,较低的pH和较高的初始Cr(Ⅵ)浓度对该菌还原Cr(Ⅵ)具有促进作用.     

铬对中国林蛙蝌蚪生长发育的毒性效应

为评价水域环境中铬元素对两栖动物幼体的急性毒性,将中国林蛙(Rana chensinensis)28～29期蝌蚪分别暴露于30～35 mg·L-1Cr(Ⅲ)6个不同浓度和10 ～ 45mg·L-1Cr(Ⅵ)6个不同浓度的水体中,分别在24、48、72和96 h统计蝌蚪的死亡率及半致死浓度(LC50).结果表明:暴露24、48、72和96 h,Cr(Ⅲ)对蝌蚪的LC50分别为34.09±1.06、33.47±0.65、32.58±0.11和(32.05±0.20) mg·L-1,安全浓度(SC)为(3.21±0.02)mg·L-1;Cr(Ⅵ)对蝌蚪的LC50分别为91.97±5.32、51.19±4.62、35.79±1.40和(28.81±1.87) mg·L-1,安全浓度(SC)为(2.88±0.19) rng·L-1.观察表明:Cr(Ⅲ)的急性毒性是通过与蝌蚪皮肤表面的分泌物结合后粘附在鳃部,导致呼吸障碍致死;而Cr(Ⅵ)的强氧化性可导致蝌蚪的表皮溃变,鳃部萎缩致死;另外,将28～29期蝌蚪暴露于安全浓度(SC)以下的含铬水体进行慢性实验,通过检测蝌蚪的体长、体重和完全变态时间显示,低浓度的Cr(Ⅲ)和Cr(Ⅵ)对蝌蚪的生长发育仍具有一定的抑制作用,并可导致畸型发生,其作用强度呈现剂量效应,但时间累积效应不规律.     

不同体质量和饥饿程度对红鳍东方鲀幼鱼游泳能力的影响

为了考察不同体质量和饥饿程度红鳍东方鲀(Takifugu rubripes)幼鱼的游泳能力,利用行为生态学方法测定了不同体质量(0.22—3.31 g)和饥饿天数(1d、3d、6d和9d)下红鳍东方鲀幼鱼的绝对临界游速(U_crit,cm/s)、相对临界游速(U_crit’,体长/s,BL/s)、偏好游速(U_pref,cm/s)、6个流速区域(2—36 cm/s)下停留时间百分比(P_t,%)、偏好区域平均流速(V_mean,cm/s)和总游泳距离(D_1h,m)等游泳行为指标。结果显示,体质量和饥饿显著影响红鳍东方鲀幼鱼的U_crit、U_crit’、P_t、V_mean和D_1h。随体质量增加,实验鱼的U_crit、U_pref、V_mean和D_1h均逐渐升高,而U_crit...     

微生物铬转化和抗性机制与生物修复研究进展

铬(Chromium,Cr)是过渡金属元素,在自然界中以六价[CrO_4~(2-),Cr_2O_7~(2-),Cr(Ⅵ)]和三价[Cr(OH)_3,Cr(Ⅲ)]为主。很多微生物在长期铬胁迫的条件下,进化出了一系列铬转化和抗性机制。微生物对铬的转化包括Cr(Ⅵ)的还原和Cr(Ⅲ)的氧化。微生物的Cr(Ⅵ)还原可以将毒性强的六价铬转化为毒性弱或无毒的三价铬,这类微生物有较强的土壤和水体铬污染治理潜力。Cr(Ⅲ)的氧化也在铬的生物地球化学循环过程中起着至关重要的作用。除了Cr(Ⅵ)的还原,微生物对铬的抗性机制还有:(1)减少摄入;(2)外排;(3)清除胞内氧化压力;(4)DNA修复。本文主要介绍微生物的铬转化和抗性机制,以及其在铬污染生物修复中应用的最新研究进展。     

饲喂不同浓度黄曲霉毒素B1饲料对草鱼幼鱼生长和毒素积累的影响

以含不同浓度黄曲霉毒素B₁(AFB₁)(0、10、20、100、1000和5000 μg/kg饲料)的6种等氮等能(32.96%蛋白质, 14.55 kJ/g能量)配合饲料饲喂平均初始体质量为(2.90±0.16) g草鱼(Ctenopharyngodon idellus)幼鱼84d, 探讨AFB₁对草鱼幼鱼生长、肝胰脏和肾脏组织结构以及鱼体肌肉中的毒素积累的影响。实验分为6个实验组, 每组3个平行。结果表明, 在整个实验过程中各实验组幼鱼的行为均未表现出异常, 各组幼鱼的存活率、终末体重、摄食率、特定生长率、饲料效率、肝体比、脏体比均无显著差异。饲料AFB₁水平对草鱼幼鱼血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、碱性磷酸酶(AKP)、超氧化物岐化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性均无显著影响。各毒素组和对照组肝胰脏、肾脏组织学观察中未发现病理变化。摄食AFB₁≤1000 μg/kg的草鱼幼鱼肌肉中未检测出AFB₁残留, 仅在5000 μg/kg实验组中检测出肌肉中含有(1.21±0.18) μg/kg的AFB₁, 低于FDA食品安全限定标准。由此可见, 草鱼幼鱼至少可耐受AFB₁含量达5000 μg/kg饲料(实测值: 4979.2 μg/kg饲料) 84d。     

异化铁还原细菌LQ25还原重金属Cr(Ⅵ)的特性研究

【背景】异化铁还原细菌能够在还原Fe(Ⅲ)的同时将毒性较大的Cr(Ⅵ)还原成毒性较小的Cr(Ⅲ),解决铬污染的问题。【目的】基于丁酸梭菌(Clostridiumbutyricum)LQ25异化铁还原过程制备生物磁铁矿,开展异化铁还原细菌还原Cr(Ⅵ)的特性研究。【方法】构建以氢氧化铁为电子受体和葡萄糖为电子供体的异化铁培养体系。菌株LQ25培养结束时制备生物磁铁矿。设置不同初始Cr(Ⅵ)浓度(5、10、15、25和30mg/L),分别测定菌株LQ25对Cr(Ⅵ)还原效率以及生物磁铁矿对Cr(Ⅵ)的还原效率。【结果】菌株LQ25在设置的Cr(Ⅵ)浓度范围内都能良好生长。当Cr(Ⅵ)浓度为15 mg/L时,在异化铁培养条件下,菌株LQ25对Cr(Ⅵ)的还原率为63.45%±5.13%,生物磁铁矿对Cr(Ⅵ)的还原率为87.73%±9.12%,相比菌株还原Cr(Ⅵ)的效率提高38%。pH变化能影响生物磁铁矿对Cr(Ⅵ)的还原率,当pH2.0时,生物磁铁矿对Cr(Ⅵ)的还原率最高,几乎达到100%。电子显微镜观察发现生物磁铁矿表面有许多孔隙,X-射线衍射图谱显示生物磁铁矿中Fe(II)的存在形式是Fe(OH)_2。【结论】基于异化铁还原细菌制备生物磁铁矿可用于还原Cr(Ⅵ),这是一种有效去除Cr(Ⅵ)的途径。     

氮锌配施对小麦锌转运、分配与累积的影响

通过田间试验,研究不同氮锌肥运筹方式对小麦植株不同器官中锌的转运、分配与累积的影响。结果表明: 不同处理植株器官中锌浓度和锌累积量的差异达显著水平。与N₃(120 kg·hm^-2)相比,N₁(240 kg·hm^-2)和N₂(180 kg·hm^-2)的籽粒锌浓度分别提高22.0%和8.9%;与未施锌(CK)相比,ZnS(土施锌肥)、ZnF(喷施锌肥)和ZnS+ZnF(土施结合喷施锌肥)处理的籽粒锌浓度分别提高15.4%、60.5%和72.8%,籽粒锌累积量分别提高21.3%、82.5%和102.4%。籽粒中锌主要来自花后吸收锌的再分配,在ZnF和ZnS+ZnF处理中的累积贡献率分别为89.9%和100.0%,锌肥回收率分别较ZnS提高4.8和1.1倍,锌肥利用率分别提高7.9和2.2倍。当前生产条件下,当施氮量<240 kg·hm^-2时,小麦不同器官锌浓度和锌累积量均随施氮量的增加而提高,喷施锌肥可显著提高籽粒中的锌浓度和锌累积量。因而,生产中可通过维持高产施氮方案并结合生育后期喷施锌肥的措施来提高籽粒中的锌浓度和锌累积量,从而提高小麦籽粒锌营养品质。     

催化极谱法测定血清中总铬量

pH=9.3时,铬(Ⅵ)在邻二氮菲——亚硝酸钠体系中,有一灵敏的极谱催化波,检测下限为0.05ppb,在0.05—2.5ppb之间有良好的线性关系。可准确用于定量。Cr(Ⅲ)氧化为Cr(Ⅵ)后,可测得总铬量。     

水环境中Cr(Ⅵ)对鱼类毒性机理研究进展

随着工业,特别是不锈钢产业的迅速发展,环境中的铬污染问题日益严重,Cr(Ⅵ)能够很容易地透过细胞膜进入细胞和生物体内,其毒性远高于Cr(Ⅲ).铬作为变价金属,其在鱼类体内能够产生活性氧自由基(ROS),对机体产生氧化胁迫效应;此外,Cr(Ⅵ)在细胞还原作用下生成的中间产物\[Cr(Ⅴ)、Cr(Ⅳ)等\]会进一步和DNA结合,导致基因的损伤和突变,从而危害鱼类的生长发育和种群结构.本文在不同水平上,系统总结了Cr(Ⅵ)对鱼类的毒性效应,从多个层次(分子、细胞、组织、器官、个体）阐述了Cr(Ⅵ)的毒性作用机制和鱼类相应的毒性解毒机制,并对于Cr(Ⅵ)的毒性研究中尚不完全清楚、需要深入考察的方面进行了探讨.     

Dietary supplementation of organic or inorganic chromium modulates the immune responses of broilers vaccinated with Avian Influenza virus vaccine

Dietary supplementation with the organic chromium (Cr) has been shown to positively affect the immune function of poultry. However, to our knowledge, no experiment has been done to directly compare the impacts of Cr chloride and chromium picolinate (CrPic) on the immune responses of broilers vaccinated with Avian Influenza (AI) virus vaccine. Therefore, the present experiment was conducted to investigate the effects of supplemental Cr sources (Cr chloride and CrPic) and levels on the growth performance and immune responses of broilers vaccinated with AI virus vaccine so as to provide an effective nutritional strategy for improving immune function of broilers. A total of 432 1-day (d)-old male broiler chicks were used in a 1 plus 2×4 design. Chickens were given either a diet without Cr supplementation (control) or diets supplemented with 0.4, 0.8, 1.6, or 3.2 mg Cr/kg as either Cr chloride or CrPic for 42 d. Compared to the control, dietary Cr supplementation had no effect (P>0.05) on average daily gain, average daily feed intake and gain : feed of broilers during the starter and grower phases, but increased (P<0.05) the relative weights of bursa of fabricius on d 21 and thymus, spleen, or bursa of fabricius on d 42, serum antibody titers against AI virus on d 21, 28, 35 and 42, blood T-lymphocyte transformation rate on d 28 and 42, blood T-lymphocyte percentage on d 42, and serum interleukin-2 contents on d 28. Broilers fed the diets supplemented with the inorganic Cr chloride had higher (P<0.05) weights of thymus, spleen and bursa of fabricius than those fed the diets supplemented with the CrPic on d 42. In addition, broilers fed the diets supplemented with the CrPic had higher (P<0.05) antibody titers against AI virus than those fed the diets supplemented with the inorganic Cr chloride on d 21 and 35. These results indicate that dietary Cr supplementation improved immune responses of broilers vaccinated with AI virus, and the inorganic Cr chloride was more effective than the CrPic in increasing the relative weights of lymphoid organs, however, the CrPic was more effective than the inorganic Cr chloride in enhancing the serum antibody titer against AI virus.     

六价铬在斜带石斑鱼胚胎中的生物累积及其对igf2、glut2和pparg基因表达的影响

以斜带石斑鱼(Epinephelus coioides)为研究对象, 探讨了水中不同浓度梯度六价铬(0、0.20、0.60、1、5、10、20、40、60和80 mg/L)在胚胎发育不同阶段(桑葚期、囊胚期、原肠末期、脑泡形成期和心脏跳动期)的生物累积及其对细胞生长基因igf2和营养代谢基因glut2、pparg的mRNA表达的影响。结果表明, 胚胎中Cr6+生物累积量和吸收率随暴露浓度的增加而增加, 且吸收率随胚胎发育时期的延伸而降低。在桑葚期时, 斜带石斑鱼胚胎吸收Cr6+能力最强, 是心脏跳动期的20倍。在桑葚期、囊胚期和原肠末期, Cr6+对胚胎中igf2和glut2基因mRNA表达水平有显著促进作用(P<0.05), 但对pparg基因mRNA表达水平有显著抑制作用(P<0.05)。在原肠末期和脑泡形成期, Cr6+对胚胎中pparg基因mRNA表达水平有显著促进作用(P<0.05)。研究表明水中Cr6+暴露在斜带石斑鱼胚胎发育过程中有明显的生物累积, 且对细胞生长水平和营养代谢有明显的影响, 研究为斜带石斑鱼早期生活史阶段适宜生境和资源保护提供了理论基础。     

Effects of dietary chromium picolinate and peppermint essential oil on growth performance and blood biochemical parameters of broiler chicks reared under heat stress conditions

A study was conducted using 240 female day-old broiler chicks to evaluate the effects of dietary chromium picolinate (CrPic), peppermint essential oil (P.mint), or their combination on growth performance and blood biochemical parameters of female broiler chicks raised under heat stress conditions (HS, 23.9 to 38 °C cycling). Average daily gain (ADG), average daily feed intake (ADFI), and feed conversion ratio (FCR) were obtained from 1 to 42 days of age. Furthermore, at the end of the experiment (day 42), birds were bled to determine some blood biochemical parameters and weighed for final body weight (BW). ADFI, ADG, and BW were not influenced significantly by dietary CrPic and P.mint (P?>?0.05). A significant interaction between dietary CrPic and P.mint on FCR (P?=?0.012) was detected. FCR significantly decreased in chicks fed the diet including both CrPic and P.mint compared with the CrPic group. Significant interaction between dietary P.mint and CrPic on serum concentrations of triglycerides, glucose, and albumin were observed (P?<?0.05), but the other measured blood biochemical parameters were not statistically affected by dietary treatments (P?>?0.05). The serum concentrations of glucose, triglycerides were decreased (P?<?0.05) in broilers fed the diet including both CrPic and P.mint. Plasma chromium (Cr) content increased significantly (P?<?0.05) in birds fed the CrPic-included diet compared with the control group (P?<?0.05). From the results of the present experiment it can be concluded that dietary supplementation with combined P.mint and CrPic could have beneficial effects on some blood biochemical parameters of female chicks reared under heat stress conditions.     

Chromium Picolinate Modulates Serotonergic Properties and Carbohydrate Metabolism in a Rat Model of Diabetes

Chromium picolinate (CrPic) has shown both antidepressant and antidiabetic properties. In this study, the effects of CrPic on serotonergic properties and carbohydrate metabolism in diabetic rats were evaluated. Sixty male Sprague-Dawley rats were divided into four groups. (1) The control group received only standard diet (8?% fat). (2) The CrPic group was fed standard diet and CrPic (80?μg CrPic per kilogram body mass (b.m.)/day), for 10?weeks (microgram/kilogram b.m./day). (3) The HFD/STZ group fed a high-fat diet (HFD, 40?% fat) for 2?weeks and then received streptozotocin (STZ, 40?mg/kg, i.p.) (i.v.) HFD-STZ-CrPic group treated as the previous group and then were administered CrPic. CrPic administration to HFD/STZ-treated rats increased brain chromium levels and improved all measurements of carbohydrate metabolism and serotonergic properties (P?相似文献   

Ultrastructural damage in chromium picolinate-treated cells: a TEM study

Chromium picolinate (CrPic) is a human dietary supplement that provides a bioavailable form of chromium(III). Its mechanism of action is unknown, and a number of toxic endpoints have been attributed to its use. Understanding the cellular effects of CrPic is important for confirmation or dismissal of these potential toxic effects. The purpose of this work was to characterize morphological damage caused by CrPic, picolinic acid, and chromic chloride in Chinese hamster ovary AA8 cells. A 48-h exposure to 80 micro g/cm(2) CrPic (0.44 mg/mL CrPic) produced 45% survival by colony formation. Transmission electron microscopy (TEM) showed 83% of analyzed cells having swollen mitochondria with degraded cristae. Apoptosis was identified by nuclear convolution and fragmentation, and cytoplasmic blebbing. Apoptosis was quantified by fluorescence microscopy with acridine orange/ethidium bromide staining. At the 80 micro g/cm(2) dose of CrPic, 37% of the cells were apoptotic cells at 48 h. An equivalent dose of picolinate, 3 mM, was much more cytotoxic and thus there was an inadequate cell number for TEM analysis. However, a lower dose of 1.5 mM induced 49% cell survival, and damaged 86% of the mitochondria, with 51% of the cells undergoing apoptosis. A dose of 1 mM chromic chloride produced 71% cell survival, and damaged 86% of the mitochondria, with 22% of the cells undergoing apoptosis. The amount of apoptosis correlated with overall cell survival by colony formation, but not with the amount of mitochondrial damage. The coordination of Cr(III) by picolinate ligands may alter the cellular chemistry of Cr(III) to make chromium picolinate a toxic form of Cr(III).     

The Effects of Chromium Picolinate and Chromium Histidinate Administration on NF-κB and Nrf2/HO-1 Pathway in the Brain of Diabetic Rats

The objective of this experiment was to investigate the effects of supplemental chromium picolinate (CrPic) and chromium histidinate (CrHis) on nuclear factor-kappa B (NF-??B p65) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling pathway in diabetic rat brain. Nondiabetic (n?=?45) and diabetic (n?=?45) male Wistar rats were either not supplemented or supplemented with CrPic or CrHis via drinking water to consume 8???g elemental chromium (Cr) per day for 12?weeks. Diabetes was induced by streptozotocin injection (40?mg/kg i.p., for 2?weeks) and maintained by high-fat feeding (40?%). Diabetes was associated with increases in cerebral NF-??B and 4-hydroxynonenal (4-HNE) protein adducts and decreased in cerebral nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha (I??B??) and Nrf2 levels. Both Cr chelates were effective to decrease levels of NF-??B and 4-HNE protein adducts and to increase levels of I??B?? and Nrf2 in the brain of diabetic rats. However, responses of these increases and decreases were more notable when Cr was supplemented as CrHis than as CrPic. In conclusion, Cr may play a protective role in cerebral antioxidant defense system in diabetic subjects via the Nrf2 pathway by reducing inflammation through NF-??B p65 inhibition. Histidinate form of Cr was superior to picolinate form of Cr in reducing NF-??B expression and increasing Nrf2 expression in the brain of diabetic rats.     

Effect of different doses of chromium picolinate on protein metabolism in infant rats.

This 12-day study was conducted to evaluate the effects of three different levels of dietary chromium (100, 200, and 500 microg/day) in the form of chromium picolinate (CrPic) on growth and protein use in weaned rats. No significant effect of CrPic on body weight gain, food intake, or food conversion rate was observed. Elevated doses of CrPic seemed to increase muscle mass, either by stimulating protein anabolism by activation of insulin by chromium or by lowering protein degradation. However, these effects had no repercussions on overall growth, suggesting that any anabolic effect of chromium due to the action of insulin was probably marginal.     

Chromium(III) tris(picolinate) is mutagenic at the hypoxanthine (guanine) phosphoribosyltransferase locus in Chinese hamster ovary cells.

Chromium trispicolinate (CrPic) is a popular dietary supplement that is not regulated by the Food and Drug Administration. We are using this compound as a bio-available model to explore the role of Cr(III) in Cr(VI)-induced cancers. The ability of CrPic to cause mutations at the hypoxanthine (guanine) phosphoribosyltransferase (hprt) locus of CHO AA8 cells has been measured after a 48 h exposure. The highest dose tested was 80 microg/cm(2) CrPic, which, if fully soluble, would be equivalent to 1mM or 0.44 mg/ml CrPic, and would correspond to 1mM Cr(III) or 52 microg/ml Cr(III). This exposure resulted in 68+/-16% cell survival based on 48 h cell counts, and 24+/-11% survival by 7-day colony formation. Exposure of CHO cells to CrPic produced a statistically significant increase in 6-thioguanine (6-TG)-resistant cells over the dose range tested. The 80 microg/cm(2) CrPic exposure resulted in an average induced mutation frequency (MF) of 58 per 10(6) surviving cells, or an average 40-fold increase in hprt mutants relative to untreated cells. An equivalent dose of 3mM Pic was highly cytotoxic and did not yield hprt mutants. The dose range of 0.375-1.5mM Pic produced a slight increase in hprt mutants, but the increase was not statistically significant. An equivalent dose of 1mM chromic chloride yielded an induced MF of 9 per 10(6) surviving cells, or a 10-fold increase in mutants with cell survivals of >100%. The coordination of Cr(III) with picolinic acid may make the metal more genotoxic than other forms of Cr(III). In light of the current results and the known ability of Cr(III) and CrPic to accumulate in tissues, as well as the growing evidence of Cr(III) involvement in Cr(VI)-induced cancers, we caution against ingestion of large doses of CrPic for extended periods.     

Movement and bioaccumulation of chromium in an artificial freshwater ecosystem

In the present study, a small fresh water aquatic ecosystem was created into a small test tank to evaluate the movement and bioaccumulation of Cr (VI) through water, sediment, a macrophyte Hydrilla, small fish guppy, and few key organs of magur, Clarias batrachus. The Cr (VI) intoxication was imposed of as a single dose of 30 mg/l concentration for a wide range of exposure durations like 1, 7, 14 and 21 days. After 1 day of exposure the total Cr (VI) load was very high in the water and sediment samples (5.187 microg/ml and 23.332 microg/g respectively) which were decreased with increasing exposure durations over their respective controls. In samples of macrophyte, Cr (VI) concentration showed a gradual increasing trend from 6.1797 microg/g in control to 21.1903 microg/g in 1 day exposure and reached up to 24.635 microg/g after 21 days exposure. In guppy, the Cr (VI) bioaccumulation showed an increasing trend but the rate was not statistically significant. However, in magur, the Cr (VI) uptake showed a significant gradual and increasing trend with increasing exposure durations in liver, brain, intestine and muscular tissues than gill and kidney over their respective controls. The movement of the Cr (VI) was found to be from sediment to water during pre-treatment phase, after intoxication, from water to macrophyte and to other phytoplankton and zooplankton. It then accumulated in the primary consumer guppy and finally moved to the secondary consumer the magur following the food web. The results reveal that the rate of movement and bioaccumulation of Cr (VI) varied from organism to organism and in C. batrachus, from tissue to tissue.