Pb2+、Cd2+和Ce3+对猪胰α-淀粉酶活性的影响

分别研究了Pb2+、Cd2+和Ce3+对Ca(Ⅱ) α-淀粉酶活性影响及对其Ca2+的竞争作用.结果表明三种金属离子低浓度情况下(0.5～5 mmol/L)对α-淀粉酶具有激活现象,而较高浓度则抑制酶活力.Pb2+、Cd2+和Ce3+竞争置换α-淀粉酶中Ca2+能力的大小是:Pb2+＞Cd2+＞Ce3+,其抑制酶活作用大小:Pb2+＞Cd2+＞Ce3+.     

NAD^+与细胞衰老

烟酰胺腺嘌呤二核苷酸(nicotinamide adenine dinucleotide,NAD^+)作为糖酵解、三羧酸循环和氧化磷酸化中关键酶的辅助因子,参与了细胞的物质代谢、能量合成、损伤DNA的修复等多种生理病理过程。近年来越来越多的研究发现,细胞内NAD^+水平在机体或细胞衰老过程中呈明显下降趋势,而补充NAD^+能延缓细胞/机体的衰老,使NAD^+及其前体物质在细胞衰老中的作用受到广泛关注。该文就NAD^+及其前体物质与细胞代谢、衰老的关系及相关分子机制研究的最新进展进行综述,以期深入认识NAD^+与细胞衰老的内在联系,为细胞衰老相关的基础及应用研究提供理论参考。     

Cu2+、Pb2+胁迫对秋茄幼苗可溶性蛋白和抗氧化酶活性的影响

【摘要】为研究重金属胁迫对秋茄幼苗抗氧化系统的影响, 砂培红树植物秋茄幼苗一个月,研究不同重金属浓度(Cu2+: 0、3、15、30、45 mg·L–1, Pb2+: 0、1、5、10、15 mg·L–1)和不同实验时间(0、3、7、14、28 d)对叶片的影响。测量的生理指标包括: 可溶性蛋白、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和过氧化物酶(POD), 实验条件下两种重金属对各项参数的影响一致。结果表明: 在特定浓度重金属处理下(Cu2+: 0、3、15、30、45 mg·L–1, Pb2+: 0、1、5、10、15 mg·L–1), 可溶性蛋白含量随着时间的增加基本呈先升后降趋势; SOD活性呈降低趋势; CAT活性最初受到明显促进, 后促进作用减弱; POD活性变化规律并不一致。在相同处理时间下, 可溶性蛋白含量随Cu2+浓度的增加而降低, 在Pb2+处理下有所波动; SOD活性在各浓度条件下均降低; CAT活性基本呈降低趋势; POD活性呈先升后降的趋势。通过Pearson相关性分析和PCA分析表明, 可溶性蛋白含量与SOD、POD、CAT三种酶活性呈显著负相关关系, 相关系数分别为–0.401, –0.722, –0.521; 而SOD、POD和CAT活性则表现为显著正相关关系, SOD与POD的相关系数为0.359, SOD与CAT的相关系数为0.384, POD与CAT的相关系数为0.485, 说明三种抗氧化酶协同作用形成一条抗氧化链抵御重金属胁迫。     

在核苷酸三磷酸酶活化过程中核苷酸与Na~+之间的关系

<正> Na~++K~+-ATP酶反应序列包括依赖Na~+的磷酸化作用及依赖K~+的去磷酸化作用。具体包括五部分反应:1.Na~+和ATP与酶的高亲和结合部位任意结合;2.依赖Na~+和Mg~(++)的磷酸化反应,此步被ADP所抑制;3.从对ADP敏感的E_1～P转化成对K~+敏感的E_2-P;4.在K~+刺激下使E_2-P水解,释放无机磷;5.核苷酸促使E_2K→E_1K转换。 为探讨膜结合Na~+和K~+激活的核苷酸三磷酸酶活性及依赖Na~+的磷酸化反应的核苷酸特异性,我们选用ATP、CTP、ITP和GTP四种核苷酸做底物,观察Na~+与核苷酸的关系。     

Cr6+、Cr3+胁迫对黑藻生理生化影响的比较研究

以沉水植物黑藻 (Hydrillaverticillata(L .f.)Royle)为实验材料 ,通过模拟水体Cr6+ 、Cr3 + 污染环境 ,比较研究了两种价态铬对黑藻叶的毒害影响。结果表明 :随着Cr6+ 、Cr3 + 浓度的加大 ,超氧阴离子 (O 2)产生速率、丙二醛 (MDA)、可溶性蛋白含量皆呈先升后降趋势。Cr6+ 、Cr3 + 浓度过高时 ,三种抗氧化酶 (SOD、POD、CAT)活性比例失衡 ,且Cr6+ 处理组的O 2 产生速率、MDA含量高于Cr3 + 处理组 ,叶绿素、可溶性蛋白含量、叶绿素a/b值低于Cr3 + 处理组 ,显示出Cr6+ 的毒性远大于Cr3 + 。     

Ca2+预处理对热胁迫下辣椒叶肉细胞中Ca2+-ATP酶活性的影响

在常温下生长的辣椒(Capsicum annum L.)叶肉细胞中Ca2+-ATP酶主要分布于质膜、液泡膜上,叶绿体的基质和基粒片层上也有少量分布;在40℃下热胁迫不同的时间,酶活性逐渐下降,直至叶绿体超微结构解体.同样条件下,经过Ca2+预处理后,分布在上述细胞器膜或片层上的酶活性大大提高,表明Ca2+预处理对该酶活性具有激活作用;Ca2+预处理对热胁迫下的超微结构的完整性具有一定的保护作用,并且能使Ca2+-ATP酶在热胁迫下维持较高活性.结果表明,Ca2+预处理增强辣椒幼苗的抗热性,可能与其稳定细胞膜、从而使Ca2+-ATP酶在热胁迫下保持较高活性有一定关系.     

Hg2+和Cd2+胁迫对满江红生理和细胞超微结构的影响

研究了在梯度浓度Hg2+和Cd2+胁迫下,满江红(Azolla imbricata (Roxb.) Nakai)的叶绿素含量、叶绿素a/b比值、光合放氧速率、呼吸速率、抗氧化酶系(超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、过氧化物酶(POD))和细胞超微结构受Hg2+和Cd2+的毒害影响.结果显示:随着胁迫程度的增大,叶绿素含量、叶绿素a/b比值、光合放氧速率明显下降,呼吸速率均在2 mg/L浓度下达到峰值,尔后下降; SOD、CAT、POD的活性均出现不同程度的应激性升高(除POD在Cd2+处理时下降),尔后下降.电镜观察发现,随着污染物浓度的增加和胁迫时间的延长,叶绿体出现膨大、破损和解体;线粒体嵴突膨胀和线粒体变形及空泡化;核染色质凝集,核仁消失,核膜破裂.实验结果表明: Hg2+和Cd2+污染不仅损害植物的生理活性,而且也破坏细胞的超微结构,最终导致植物死亡;随着Hg2+和Cd2+胁迫的增大,细胞超微结构的损伤程度和植物的生理变化是同步的;植物受毒害的程度表现出明显的剂量效应关系;在同一处理时间和浓度下,Cd2+对满江红的毒性大于Hg2+.Hg2+对满江红的致死浓度为3.5～4.0 mg/L,Cd2+为3.0～3.5 mg/L.对满江红鱼腥藻(Anabaena azollae Strasburger)细胞的超微结构变化观察表明,满江红鱼腥藻对Hg2+和Cd2+的耐受性明显高于满江红.     

燕麦根细胞质膜K+刺激ATP酶的纯化(英文)

Triton X-100加KI能够有效地溶解燕麦根细胞质膜上K~+刺激的ATP酶(张堃等1989)。对这种溶解的K~+刺激的ATP酶进行甘油梯度离心,得到了一些结果:1.在pH 7.5甘油梯度离心,溶解的ATP酶活性损失约85％,在pH 4.5时活性仅损失约50％,这表明低pH条件对于ATP酶活性稳定的重要性,2.使用水平转子进行甘油梯度离心效果较好;3.甘油梯度离心纯化的ATP酶经SDS-PAGE分析,85％以上的酶蛋白分子量为34kD的多肽。这一低分子量的具有K~+刺激的ATP酶活性的多肽与100kD左右的ATP酶(Serrano 1984)之间的关系有待进一步研究;4.经甘油梯度离心纯化后,K~+刺激的ATP酶活性占K~+,Mg~(2+)-ATP酶活性的52％;而溶解的ATP酶活性中,K~+刺激的部分仅为35％(表1)。此结果类似透析对溶解的ATP酶的影响(张堃等1989)。表明溶解的ATP酶制剂中K~+的存在掩盖了K~+对ATP酶的刺激作用。     

纳米TiO2、ZnO、SiO2对剑尾鱼肝组织中Na+/K+-ATP酶活性的影响

采用浸浴法研究了氧化纳米颗粒TiO2、ZnO、SiO2对剑尾鱼(Xiphophorus helleri)肝中Na+/K+-ATP酶活性的影响。结果表明:纳米TiO2处理组,高浓度(5 mg/L、10 mg/L)组表现为抑制作用,其中5 mg/L处理组Na+/K+-ATP酶的活性与对照组无显著差异(p>0.05),10 mg/L处理组中Na+/K+-ATP酶的活性显著低于对照组中酶的活性(p<0.05)。低浓度组(0.1 mg/L、1 mg/L)则表现为先诱导后抑制,除0.1 mg/L组在暴露1 d后与对照组有显著差异外(p<0.05),其余组与对照组均无显著差异(p>0.05)。纳米ZnO、SiO2处理组(0.1 mg/L、10 mg/L)在暴露1 d后,肝中Na+/K+-ATP酶的活性均比对照组高,随着暴露时间增加至20 d,Na+/K+-ATP酶活性下降,且显著低于对照组(p<0.05)。3种纳米颗粒的浓度为0.1 mg/L时,对暴露后1 d剑尾鱼肝中的Na+/K+-ATP酶活性的影响均为诱导作用,诱导大小顺序为ZnO>TiO2>SiO2;随着暴露时间的增加至10 d,纳米TiO2、ZnO、SiO2处理组对Na+/K+-ATP酶活性均表现出抑制作用。     

Pb2+、Cd2+和Ce3+对猪胰α-淀粉酶活性的影响

分别研究了Pb²⁺、Cd²⁺和Ce³⁺对Ca(Ⅱ) α-淀粉酶活性影响及对其Ca²⁺的竞争作用.结果表明三种金属离子低浓度情况下（0.5～5 mmol/L）对α-淀粉酶具有激活现象,而较高浓度则抑制酶活力.Pb²⁺、Cd²⁺和Ce³⁺竞争置换α-淀粉酶中Ca²⁺能力的大小是：Pb²⁺＞Cd²⁺＞Ce³⁺,其抑制酶活作用大小：Pb²⁺＞Cd²⁺＞Ce³⁺.     

Synthesis, structural characterization and antimicrobial activities of 4- and 6-coordinate nickel(II) complexes with three thiosemicarbazones and semicarbazone ligands

To investigate the relationship between antimicrobial activities and the molecular structures of nickel(II) complexes with thiosemicarbazone and semicarbazone ligands, nickel(II) complexes with ligands Hmtsc, Hatsc, Hasc and H2dmtsc, were prepared and characterized by elemental analysis, FT-IR, 1H and 13C NMR spectroscopies, magnetic susceptibility measurements, UV-Vis absorption spectra, TG/DTA and single-crystal X-ray analysis. Their antimicrobial activities were evaluated by the MIC against four bacteria (B. subtilis, S. aureus, E. coli and P. aeruginosa), two yeasts (C. albicans and S. cerevisiae) and two molds (A. niger and P. citrinum). The 4-coordinate, diamagnetic nickel(II) complexes showed antimicrobial activities which were different from those of free ligands or the starting nickel(II) compounds; [Ni(mtsc)(OAc)] 1 showed selective and effective antimicrobial activities against two Gram-positive bacteria (B. subtilis and S. aureus) and modest activities against a yeast (S. cerevisiae), [Ni(mtsc)Cl] 3 exhibited moderate activities against a Gram-positive bacterium (S. aureus), and [Ni(atsc)(OAc)] 5 showed modest activities against two Gram-positive bacteria (B. subtilis and S. aureus). On the other hand, the 6-coordinate, paramagnetic nickel(II) complexes with two protonated or deprotonated ligands ([Ni(mtsc)2] 2, [Ni(atsc)(mtsc)] 4, [Ni(atsc)2] 6, [Ni(Hatsc)2](NO3)(2)7, [Ni(Hatsc)2]Cl(2)8 and [Ni(Hasc)2](OAc)(2)9) and the sterically crowded 4-coordinate, diamagnetic nickel(II) complex ([Ni(dmtsc)] 10) did not inhibit the growth of the test organisms. The structure-activity correlation in this series of nickel(II) complexes was discussed based on their ligand-replacement abilities.     

Nickel toxicity inPseudomonas tabaci: Single cell and bulk sample analysis of bacteria cultured at high cation levels

Summary The growth ofPseudomonas tabaci in nutrient medium is partially inhibited in the presence of 10^–3 M added nickel (threshold toxic concentration), with complete inhibition at 10^–2 M nickel—but no effect at 10^–4 and 10^–5 M. Toxic levels of nickel affect both cell division and cell viability.Spectrophotometric determination of intracellular levels of nickel at different external concentrations showed that the highest internal values occurred with cells cultured in 10^–4M (non-toxic) nickel medium rather than in 10^–3 (toxic) medium—suggesting that nickel toxicity does not primarily relate to internal concentration.X-ray microanalysis, carried out on whole bacterial cells, showed that toxic levels of nickel in the external medium resulted in a range of ionic changes in the cell, including a decrease in the level of K (K efflux) and an increase in the levels of Mn, Fe, Ni, and Cu (transition metal cation influx). Other changes induced by nickel toxicity included an increase in the level of soluble S (with a decrease in insoluble S), an increased cell dry mass, and a conspicuous plasmolysis—which was observed both in whole cells and in ultrathin sections.The results obtained support a primary toxic effect of nickel at the cell surface—possibly directly affecting the transport activity of the plasmalemma. The resulting changes, particularly involving the influx of a range of cations, may lead to secondary toxic activities affecting the whole metabolism, leading to plasmolysis and inhibition of division.     

Effects of the nitric oxide donor sodium nitroprusside on antioxidant enzymes in wheat seedling roots under nickel stress

The inhibitory effect of nickel on the growth of wheat (Triticum aestivum L.) seedlings and the alleviation of nickel toxicity by nitric oxide (NO) were investigated. Nickel (Ni) at 100 μM caused striking reduction in seedling growth and significant overproduction of MDA and H₂O₂ in the roots. Supplementation with NO donor sodium nitroprusside (SNP) could significantly reverse the inhibitory effect of nickel in a dose-dependent manner. K₃Fe(CN)₆, a SNP analogue, which does not release NO, had no ameliorative effect on Ni toxicity in wheat.. In addition, application of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), a NO scavenger, could dramatically counteract the stimulatory effects of SNP on the growth of wheat seedling roots under Ni stress, confirming that NO rather than other compounds derived from SNP was responsible for the alleviating effect of Ni toxicity. Further results showed that SNP enhanced the activities of guaiacol peroxidase (POD, EC 1.11.1.7), ascorbate peroxidase (APX, EC 1.11.1.11), superoxide dismutase (SOD, EC 1..1..5.1..1), glutathione reductase (GR, EC 1.6.4.2), and glutathione S-transferase (GST, EC 2.5.1.18) in wheat seedling roots under nickel stress, while no significant difference in the activity of catalase (CAT, EC 1.11.1.6) in wheat roots supplemented with SNP or without it was observed. These results clearly indicate that NO has a protective role in Ni-induced oxidative damage through modulation of antioxidant enzymes.     

Genetic and physiological characterization of new Escherichia coli mutants impaired in hydrogenase activity

The Mu dl (ApR lac) bacteriophage was used to generate mutants of Escherichia coli which were defective in formate hydrogenlyase. Three mutants were chosen for further analysis: they lacked hydrogenase (hydrogen: benzyl viologen oxidoreductase) activity, but produced normal levels of fumarate reductase activity and two- to three-fold reduced levels of benzyl viologen (BV)-dependent formate dehydrogenase activity. Two of them (hydC) were shown to contain about 4-fold reduced amounts of formate hydrogenlyase and fumarate-dependent H2 uptake activities. The third one (hydD) was totally devoid of both activities. Their insertion sites were located at 77 min on the E. coli map. Subdivision of these mutants into two classes was subsequently based on the restoration capacity of hydrogenase activity with high concentration of nickel in the growth media. Addition of 500 microM NiCl2 led to a complete recovery of hydrogenase activity, and to the concomitant restoration of normal BV-linked formate dehydrogenase, formate hydrogenlyase and fumarate-dependent H2 uptake activities in the hydC mutants. The hydD mutant was insensitive to the effect of nickel. Expression of the lac operon in hydC and hydD mutants was induced by anaerobiosis. It was not increased by the addition of formate under anaerobic conditions. The presence of nitrate resulted in slightly reduced beta-galactosidase activities in the hydC mutants, whereas those found in the hydD mutant reached only one third of the level obtained in its absence. Fumarate had no effect on both classes. Moreover, in contrast to the hydD locus, the hydC::Mu dl fusions were found to be dependent upon the positive control exerted by the nirR gene product and were totally repressed by an excess of nickel. In addition, the low levels of overall hydrogenase-dependent activities found in a nirR strain were also relieved by the presence of nickel. Our results strongly suggest that the pleiotropic regulatory gene nirR is essential for the expression of a gene (hydC) involved in either transport or processing of nickel in the cell, whose alteration leads to a loss of hydrogenase activity.     

镍处理对水稻叶片H_2O_2 积累和抗病的诱导效应

2 .2 0mmol/L的硝酸镍处理水稻幼苗后第 3天用稻白叶枯菌 (Xanthomonasoryzaepv .oryzae)挑战接种 ,硝酸镍处理的稻苗病情比对照明显减轻 ,并且叶片中过氧化物酶 (POD)活性上升 ,过氧化氢酶 (CAT)和抗坏血酸过氧化物酶 (APX)活性明显下降 ,H2 O2 和丙二醛 (MDA)含量显著增加。这些结果表明 ,H2 O2 积累与镍诱导的抗病作用密切有关     

Protective role of <Emphasis Type="SmallCaps">l</Emphasis>-ascorbic acid on antioxidant defense system in erythrocytes of albino rats exposed to nickel sulfate

In this experimental study, we investigated whether l-ascorbic acid has any influence on the blood antioxidant defense system, lipid peroxidation and hematological parameters of the albino rats exposed to nickel sulfate(NiSO₄).Twenty four adult rats were divided into four groups of six animals in each group. The control rats were untreated and comprised Group I. Group II rats were administered nickel sulfate (2.0 mg/100 g b.wt.; intraperitonially, i.p.). Group II rats were treated orally l-ascorbic acid (50 mg/100 g b.wt.) and Group IV rats were given both nickel sulfate and l-ascorbic acid simultaneously on alternate days until the tenth dose. The hematological parameters were assessed: red blood corpuscle counts, packed cell volume %, hemoglobin concentration, white blood corpuscle counts and platelets count decreased significantly and clotting time increased significantly in nickel treated rats. We also observed increase malondialdehyde (MDA) and decrease glutathione level (GSH) in erythrocytes of nickel treated rats. The activities of erythrocyte antioxidant enzymes like superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) were significantly increased in rats treated with nickel sulfate. Simultaneously treatment of l-ascorbic acid exhibited a possible protective role on the toxic effect of nickel sulfate on the hematological values, erythrocyte MDA and GSH concentrations as well as antioxidant enzymatic defense system.     

Effects of Pb2+, Ni2+, Hg2+ and Se4+ on cultured cells. Analysis of uptake, toxicity and influence on radiosensitivity

Effects of Pb²⁺, Ni²⁺, Hg²⁺ and Se⁴⁺ on cultured human glioma U-343MG cells were investigated considering uptake, toxicity and, in combination with radiation, clonogenic cell survival. The cells were exposed to 0-100 m of the metals for a week before the evaluation. The tests showed a tendency to toxicity with 10 m nickel although not significant (P > 0.05). Selenium, lead and mercury exerted a significant toxicity (P < 0.05) at 2.5 m, 10 m and 1 m, respectively. To challenge the clonogenic cell survival capacity, the cells were irradiated with⁶⁰Co photons after being exposed to the highest nontoxic concentration of the different metals. The clonogenic cell survival tests, after irradiation, showed no significant change if the cells were exposed to 5 m nickel, 0.5 m selenium or 5 m lead compared with those not exposed. Mercury, 0.1 m, gave a relative reduction in survival compared with only irradiated cells of 58 ± 17%. Thus, only mercury affected the radiation-induced damage and/or repair. When exposed to the highest nontoxic concentrations of the different metals, the cultures did not display a significant uptake ratio (metal concentration ratio of exposed cells to control cells) of nickel (3.1 ± 3.3), only a small uptake ratio of selenium (4.0 ± 0.4), while there was a large uptake ratio of both lead (2.6 ± 1.7) x 10² and mercury (1.5 ± 0.2) x 10¹. The results indicated that nickel was neither especially toxic nor influenced the clonogenic cell survival after irradiation. Mercury was more toxic and also influenced the radiation sensitivity. Lead was taken up strongly but did not influence the radiation sensitivity. Selenium accumulated but gave no detectable effect on the radiation sensitivity.     

Measurement with microelectrodes of intracellular Na+, K+, H+ and Cl- activities and of membrane potential in normal rat liver slices and during the 4-dimethylaminoazobenzene-induced rat hepatocarcinogenesis

Steady-state membrane potentials (Vm) and intracellular Na+ (aiNa), K+ (aiK), H+ (aiH) and Cl- (aiCl) activities were measured with double-barrelled ion-selective microelectrodes in liver slices from normal rats and during the 4-dimethylaminoazobenzene-induced (DAB) hepatocarcinogenesis. Rats fed with the experimental regimen without the carcinogen were used as control animals. In Krebs-Henseleit bicarbonate saline containing 5.5 mM glucose as bathing solution at 37 degrees C, Vm was found to be significantly lower in neoplastic hepatocytes, compared to normal liver cells. Vm decreased also in control rat liver cells. Increased Na+/K+ ratios and Na+ + K+ activities were found in cancerous hepatocytes whereas H+ and Cl- activities decreased. Therefore, the intracellular pH increased significantly in neoplastic cells, compared to normal and control cells. This could reflect activation of the Na+/H+ exchange system during the DAB-induced hepatocarcinogenesis, leading to a stimulation of cell metabolism with increased rate of protein and DNA synthesis and loss of growth control, under these conditions.     

Ultrastructural and cytochemical analysis of Na+, K+, ATPase and H+, K+, ATPase in parietal cells of gastric mucosa in the rabbit.

Rabbit gastric secretion has the physiological peculiarity of being continuous and uninfluenced by food intake. In this respect, ultrastructural analysis of rabbit parietal cells has revealed morphofunctional features situated between states of rest and very active acid secretion. Our cytochemical study shows that Mg2+ ATPase and ADPase activities vary from cell to cell and can even be totally absent. These activities concern either microcanaliculi or laterobasal folds or both, but never tubulovesicles. Application of the technique of Mayahara to K+ pNPP, associated or not with inhibitors (ouabain, vanadate, N-ethyl-maleimide, sodium fluoride), enabled us to confirm the coexistence of H+, K+, ATPase and Na+, K+, ATPase activities in the rabbit and to determine that these activities concern basolateral folds, microcanaliculi, hyaloplasm and tubulovesicles. The global activity of K+, pNPPase varied considerably in intensity. The results of using inhibitors suggest that proton transport ceases completely in certain cells. The signs of functional alternation found in this study are in agreement with physiological data relative to this animal.     

Role of zinc in regulating the levels of hepatic elements following nickel toxicity in rats

This study was designed to determine the protective effects of zinc on the hepatotoxicity induced by nickel in rats. Female Sprague-Dawley (SD) rats received either nickel sulfate alone in the dose of 800 mg/L nickel in drinking water, zinc sulfate alone in the dose of 227 mg/L zinc in drinking water, and nickel plus zinc or drinking water alone for a total duration of 8 wk. The effects of different treatments were studied on activities of rat liver marker enzymes like alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferases (AST) and on the status of essential elements in rat liver. The study revealed a significant increase in the activities of enzymes ALP and ALT in rats subjected to nickel treatment. Interestingly, zinc supplementation to rats treated with nickel brought back the raised activities of these enzymes to within normal limits. Further, the levels of elements in liver that include zinc, copper, selenium, and potassium were found to be significantly suppressed following nickel treatment, whereas the levels of iron and sulfur were elevated. However, zinc treatment alone did not cause any appreciable change in the concentration of these elements. To the contrary, when zinc was given to nickel-treated rats, the concentrations of zinc, copper, potassium, and phosphorus were not significantly different from that of normal controls, whereas the levels of iron, selenium, and sulfur were improved in comparison to nickel-treated rats but were not within the normal limits. The present study concludes that zinc has the ability to maintain the levels of hepatic elements and has bearing in regulating the liver functions by maintaining the activities of marker enzymes in conditions of nickel toxicity.