Influence of activator and inhibitors of Ca2+ channels on proliferative activity in Tetrahymena pyriformis infusoria

It was determined that change in DNA content in macronuclei occurs in the T. pyriformis infusoria under the influence of an activator (caffeine) and inhibitors of Ca²⁺ channels (verapamil), NiCl₂, and CdCl₂. Caffeine (10 mM) stimulates DNA synthesis. Verapamil (5 ??M), CdCl₂ (125 ??M), and NiCl₂ (100 ??M) decrease DNA content in macronuclei by 30 min after proliferative stimulation. By 4 h of incubation, there is, on average, 10% less DNA in macronuclei of Tetrahymena preprocessed with verapamil than in the control cells. The cells preprocessed with CdCl₂ and NiCl₂ differ from the control cells by lower DNA content almost at all studied periods, but they restore the level of nuclear DNA by 4 h. It is assumed that trans-mission of proliferative signals in the T. pyriformis has a Ca²⁺-dependent character.     

Distribution of various nickel compounds in rat organs after oral administration

In this study, eight kinds of nickel (Ni) compounds were orally administered to Wistar male rats and the distribution of each compound was investigated 24 h after the administration. The Ni compounds used in this experiment were nickel metal [Ni−M], nickel oxide (green) [NiO(G)], nickel oxide (black) [NiO(B)], nickel subsulfide [Ni₃S₂], nickel sulfide [NiS], nickel sulfate [NiSO₄], nickel chloride [NiCl₂], and nickel nitrate [Ni(NO₃)₂]. The solubilities of the nickel compounds in saline solution were in the following order; [Ni(NO₃)₂>NiCl₂>NiSO₄]≫[NiS>Ni₃S₂]>[NiO(B)>Ni−M>NiO(G)]. The Ni level in the visceral organs was higher in the rats given soluble Ni compounds; Ni(NO₃)₂, NiCl₂, NiSO₄, than that in the rats receiving other compounds. In the rats to which soluble Ni compounds were administered, 80–90% of the recovered Ni amounts in the examined organs was detected in the kidneys. On the other hand, the Ni concentration in organs administered scarcely soluble Ni compounds; NiO(B), NiO(G), and Ni−M were very low. The estimated absorbed fraction of each Ni compounds was increased with the increase of the solubility. These results suggest that the kinetic behavior of Ni compounds administered orally is closely related with the solubility of Ni compounds, and that the solubility of Ni compounds is one of the important factors for determining the health effect of Ni compounds.     

Thermodynamic Modeling of Poorly Complexing Metals in Concentrated Electrolyte Solutions: An X-Ray Absorption and UV-Vis Spectroscopic Study of Ni(II) in the NiCl2-MgCl2-H2O System

Knowledge of the structure and speciation of aqueous Ni(II)-chloride complexes is important for understanding Ni behavior in hydrometallurgical extraction. The effect of concentration on the first-shell structure of Ni(II) in aqueous NiCl₂ and NiCl₂-MgCl₂ solutions was investigated by Ni K edge X-ray absorption (XAS) and UV-Vis spectroscopy at ambient conditions. Both techniques show that no large structural change (e.g., transition from octahedral to tetrahedral-like configuration) occurs. Both methods confirm that the Ni(II) aqua ion (with six coordinated water molecules at R _Ni-O = 2.07(2) Å) is the dominant species over the whole NiCl₂ concentration range. However, XANES, EXAFS and UV-Vis data show subtle changes at high salinity (> 2 mol∙kg^-1 NiCl₂), which are consistent with the formation of small amounts of the NiCl⁺ complex (up to 0.44(23) Cl at a Ni-Cl distance of 2.35(2) Å in 5.05 mol∙kg^-1 NiCl₂) in the pure NiCl₂ solutions. At high Cl:Ni ratio in the NiCl₂-MgCl₂-H₂O solutions, small amounts of [NiCl₂]⁰ are also present. We developed a speciation-based mixed-solvent electrolyte (MSE) model to describe activity-composition relationships in NiCl₂-MgCl₂-H₂O solutions, and at the same time predict Ni(II) speciation that is consistent with our XAS and UV-Vis data and with existing literature data up to the solubility limit, resolving a long-standing uncertainty about the role of chloride complexing in this system.     

Antagonistic effect of magnesium chloride on the nickel chloride–induced inhibition of DNA replication in chinese hamster ovary cells

The degree of inhibition of semiconservative DNA replication induced by nickel chloride (NiCl₂) was analyzed by radiolabeled-thymidine incorporation alone or with cesium chloride (CsCl) density gradient centrifugation. The onset and duration of this Ni²⁺-induced inhibition was time- and concentration- dependent, but the degree of inhibition was not. A maximal reduction in the rate of DNA synthesis was observed within the first hour of treatment with 2.5 mM NiCl₂, which was the highest noncytotoxic concentration utilized. After six hours, 500 μM and 1 mM as well as 2.5 mM NiCl₂ all produced the same 50% to 60% reduction in [³H]-thymidine incorporation into DNA. The inhibitory effect of nickel ions on DNA synthesis was reversible. The rate of DNA synthesis following a 500 μM or 1 mM NiCl₂ treatment began to increase after washout of nickel, but a six-hour exposure of cells to 2.5 mM NiCl₂ produced a sustained 50% to 60% suppression of DNA synthetic activity for at least 36 hours. At all concentrations of NiCl₂ used in this study, some inhibition of DNA synthesis persisted for at least 48 hours, but by 72 hours after treatment, the rate of [³H]-thymidine incorporation was actually 10% above the control. Examination of autoradiographic slides of cells treated with 2.5 mM NiCl₂ for six hours demonstrated a 60% reduction of silver grains, but there was no preferential reduction in the quantity of grains in the nucleolus or any other region. Cesium chloride density gradient analysis of the replication of nucleolar DNA in cells treated with 2.5 mM nickel supported the autoradiographic findings. The inhibitory effect of NiCl₂ on DNA replication was prevented by the addition of magnesium chloride (MgCl₂) to cells maintained in a simple salts/glucose medium (SGM). This effect did not appear to be due to an antagonism of the cellular uptake of nickel by Mg²⁺, since the maximally effective dose of Mg²⁺ reduced ⁶³Ni²⁺ uptake by no more than 25% while the inhibition of replication was completely reversed.     

Salinity attenuates nickel-accumulating capacity of <Emphasis Type="Italic">Atropa belladonna</Emphasis> L. plants

Comparative analysis of growth and composition of Atropa belladonna L. plants was performed after separate and combined additions of NaCl and NiCl₂ to the nutrient medium. Plants were grown in water culture on modified Johnson solution for 8 weeks until the formation of the fifth leaf pair. Thereafter, NiCl₂ was introduced at final concentrations of 100 and 150 μM into the medium either separately or in combination with 100 mM NaCl. After completing the 7-day treatment with Ni ions, the plants' weight and the content of water and photosynthetic pigments were determined. The content of Ni, free polyamines (putrescine, spermidine, spermine), and atropine was determined in plant roots and leaves, whereas the content of Fe, proline, and malondialdehyde (MDA) was examined in leaves only. The distribution of Ni in various tissues was inspected using the dimethylglyoxime method. The presence of NiCl₂ in growth media diminished the increments in fresh weight of shoots and roots; lowered the content of water, pigments, and iron in leaves; and initiated chlorosis. The leaves of Ni-treated plants accumulated larger amounts of atropine, putrescine, proline, and MDA with respect to the control levels of these compounds. In contrast to the action of Ni alone, the combined application of NaCl and NiCl₂ was followed by the increased content of water and pigments in leaves. The presence of NaCl in the medium restricted the entry of Ni into roots and diminished the levels of MDA and proline in leaves. After growing the plants in the presence of 100 and 150 μM NiCl₂, nickel was located in the root outer cortex and the rhizoderm. In plants treated with 150 μM NiCl₂, nickel was also observed in tissues of the central cylinder, mostly in the pericycle, phloem, and xylem. In plants grown in the presence of 150 μM NiCl₂ and 100 mM NaCl, the decreased accumulation of nickel was noted in the tissues of the central cylinder in the root hair zone. Thus, the combined action of Ni and moderate salinity reduced nickel accumulation in roots and aboveground organs of A. belladonna plants. The reduced Ni content in plants mitigated the toxic effect of Ni present in the medium. This was manifested in stabilization of leaf water status, an increase in the content of photosynthetic pigments, and alleviation of oxidative stress, which was assessed from the content of low-molecular organic compounds exhibiting stress-protective and antioxidant action (proline, MDA, free polyamines, and atropine).     

lipid peroxidation in liver of mice administrated with nickel chloride

The relationship between Ni-induced hepatic lipid peroxidation (LPO) and the concentrations of Ni and trace elements was investigated in male ICR mice. The protective effects of antioxidants were also examined. Hepatic LPO and the concentrations of Ni, Fe, Cu, and Zn in the liver were enhanced after an ip injection of nickel chloride (NiCl₂). Dose-response studies were conducted on male mice with different groups being injected with 50, 85, and 170 μmol Ni/kg. LPO increased significantly in a dose-dependent manner. In time-course studies, mice were administrated NiCl₂ (170 μmol Ni/kg) and killed at intervals of 6, 12, 24, and 48 h after injection. Both LPO and the accumulation of Ni, Fe, Cu, and Zn in the liver showed a significantly positive time-course relationship after NiCl₂ injection. At 1 h and 24 h after a single ip injection of 170 μmol Ni/kg, the mice were given an ip injection of ascorbic acid (vit C), glutathione (GSH), and selenium (Se). Vit C and GSH significantly decreased both the level of hepatic LPO and the concentration of Ni in the liver, but did not decrease the accumulation of Fe, Cu, and Zn. However, LPO in the experimental group of mice was different significantly from that in the control group. In conclusion, the results suggest that Ni-induced hepatic LPO may result from increasing the amounts of Ni, Fe, and Cu, since these elements are involved in the generation of hydroxyl radical by inducing the Fenton reaction, thus instigating the Ni-mediated hepatic LPO. The protective effects of vit C and GSH in hepatic LPO result not only from removing the oxygen reactive species, but also from decreasing the Ni concentration.     

Phytoremediation potential of <Emphasis Type="Italic">Amaranthus</Emphasis> hybrids: Antagonism between nickel and iron and chelating role of polyamines

Three amaranth hybrids (Amaranthus paniculatus f. cruentus (Vishnevyi dzhem), A. paniculatus (Bronzovyi vek), and A. caudatus f. iridis (Izumrud) were grown in the climate-controlled chamber on Jonson nutrient medium supplemented with 2 μM Fe³⁺-EDTA. When plants developed 5–6 true leaves (six-week-old plants), NiCl₂ was added to medium to final concentrations of 0 (control), 50, 100, 150, 200, and 250 μM. In 6 days, the increment in biomass of young and mature leaves, stems, and roots, and also the contents of Ni and Fe in them were measured. The red leaf amaranth hybrid Vishnevyi dzhem manifested the highest phytoremediation potential. i.e., the highest capacity for Ni accumulation in the shoots and the most pronounced symptoms of Fe deficit. In the presence of 150 and 250 μM NiCl₂ in medium, the shoots of these plants contained about 2 and 4 mg Ni/g dry wt, respectively. In experiments with Fe deficit in plants grown for a week in the presence of NiCl₂ (0, 25, 50, 75, and 100 μM), it was established that all tested nickel concentrations suppressed iron reduction in intact roots, which is catalyzed by ferric-chelate reductase, and this may underlie the antagonism between the two metals. In the presence of 50 μM NiCl₂ in medium and 2 μM Fe³⁺ (Fe deficit) and especially 100 μM Fe³⁺ (Fe excess), the content of MDA and proline in leaves increased and superoxide dismutase was activated; this indicates a development of oxidative stress. Leaf treatment with polyamines (putrescine or spermidine) with aminoguanidine (the inhibitor of H₂O₂ generation at polyamine oxidation) and with 1,3-diaminopropane led to the increase in nickel accumulation in leaves but did not result in the appearance of any signs of injury. This confirms our previous suggestion that polyamines manifest their protectory action as Ni chelators and detoxicants.     

DNA damage induced by cigarette smoke condensate in vitro as assayed by 32P-postlabeling. Comparison with cigarette smoke-associated DNA adduct profiles in vivo.

Cigarette smoke induces a multitude of bulky/aromatic DNA adducts in vivo as revealed by 32P-postlabeling assay. The formation of such adducts is thought to involve metabolic activation of aromatic chemicals especially polycyclic aromatic hydrocarbons (PAHs) present in tumor-initiating cigarette tar fractions, via cytochrome P450-associated monooxygenases. Because radicals are present in both the gas and particulate (tar) phase of cigarette smoke and in aqueous extracts of cigarette smoke condensate (CSC), we addressed the question as to whether cytochrome P450-independent, possibly free radical-mediated reactions may contribute, also, to formation of cigarette smoke-associated bulky DNA adducts. Rat-lung DNA was incubated with aqueous extracts of CSC in the absence of microsomes under various conditions and analyzed by 32P-postlabeling. Radioactively labeled bulky reaction products were found to accumulate in a time- and CSC concentration-dependent manner. The resulting chromatographic profiles resembled cigarette smoke-associated DNA-adduct patterns observed in vivo. Pretreatment of aqueous CSC extract with radical scavengers/reducing agents (ascorbic acid, glutathione) diminished adduct formation in a concentration-dependent manner. Adduct formation in vitro may involve oxygen-free radicals, which are known to be present in aqueous CSC extracts and could (i) attack DNA directly to produce bulky adducts, (ii) induce radical sites on DNA covalently binding CSC components, or (iii) convert CSC components to DNA-reactive electrophiles. In addition, DNA may react with direct-acting mutagens in CSC. Adduct fractions derived from in vitro and in vivo experiments showed similar chromatographic behavior, suggesting that metabolic activation as well as processes not involving metabolism lead to formation of smoking-induced bulky DNA adducts in vivo.     

Chronotolerance of a Nickel (II) Complex with the 5-Methyl 2-Furaldehyde Thiosemicarbazone Ligand in Male Swiss Mice

In vitro nickel (II) complex presents antimitotic effects. In this work, we have studied the in vivo seasonal effects of nickel (II), ligand and the complex [NiCl₂(M5FTSC)₂] in male Swiss mice. During spring, an intra peritoneal (i.p.) injection of NiCl₂ in aqueous NaCl up to 1.0.10^-2 mmol.kg^-1 body weight (b.w.) killed 10% of the rodents after 6 days. Lethal dose 100% (LD100) was up 1.91.10^-2 mmol.kg^-1 b.w.; ligand was less toxic than Ni (II), while the complex was 25% lethal at 1.37.10^-2 mmol.kg^-1 b.w. In autumn, mice were less sensitive to NiCl₂. The ligand and the complex, on the contrary, were more toxic. This leads us to the conclusion that, in vivo, chronotolerance of nickel (II), ligand and complex in aqueous solution, are quite different in spring and autumn seasons.     

Genotoxic activities in vivo of cobaltous chloride and other metal chlorides as assayed in the Drosophila wing spot test

A series of metal chlorides were subjected to the wing spot test of Drosophila melanogaster. In the test, larvae trans-heterozygous for the wing-hair mutations mwh and flr were orally treated at the third instar stage with a test compound and the wings were inspected at the adult stage for spots expressing phenotypes of the markers. CoCl₂, MnCl₂, MoCl₃, NiCl₂ and ZnCl₂ were clearly effective in inducing spots with one or two mutant hairs (small spots). CoCl₂ was clearly effective in inducing spots with three or more mutant hairs (large spots) as well. CrCl₃, FeCl₂ and FeCl₃ were negative under the conditions used. Based on estimated frequencies of small spots induced at the LD₅₀, the genotoxic effectiveness of the positive metal salts were ranked in a sequence of CoCl₂ > ZnCl₂ > MoCl₃ > (MnCl₂, NiCl₂). Since CoCl₂ did not induce large spots in the wings of the mwh/TM3 flies with a suppressed ability of mitotic crossing-over, the large spots induced by this compound in the mwh/flr system were ascertained as mutant clones due to mitotic crossing-overs.     

Mutagenesis by aflatoxin in M13 DNA: Base-substitution mechanisms and the origin of strand bias

Summary The two goals of the experiments described here are: (a) to examine whether there is a strand bias in mutagenic processing of bulky lesions in M13 replicative form (RF) DNA, and (b) to examine the mutational mechanisms of metabolically activated aflatoxin. For these experiments, two types of nicked heteroduplex M13 RF DNA molecules (+WT/-am1 and +am1/-WT) in which either the minus (-) or the plus (+) strand carried a gene 1 amber nonsense codon, were constructed. Heteroduplex DNAs were modified in vitro with aflatoxin B₁ activated by hamster liver S9 enzymes, and transfected into SOS(UV)-induced Escherichia coli (Sup^o/uvrA^-/mucAB⁺). Forward mutations in the lacZ -complementing gene segment were scored and sequenced. Results indicated that aflatoxin-induced mutation frequencies in the +WT/-am1 heteroduplex were significantly greater than those in the +am1/-WT heteroduplex, suggesting more efficient mutagenic processing of lesions in the plus strand. These results permit specific suggestions for improved mutation detection in the extensively used M13 forward mutagenesis system. Sequence analysis of point mutations from the +WT/-am1 experiments showed that most substitutions were targeted to plus-strand guanines. Both G-to-A transitions and G-to-T transversions were induced with equal effeciency. Since activated aflatoxin B₁ is known to react almost exclusively with DNA guanines at the N7 position, these results suggest that bulky lesions at guanine N7 position may have the properties of mis-instructional as well as non-instructional lesions.     

Isolation and characterization of nickel-accumulating yeasts

We selected three yeast strains that efficiently remove heavy metal ions from aqueous solution. We first screened yeasts that grew in the presence of 2 mM NiCl₂ among our stock of wild yeasts, and then selected those that removed Ni most efficiently from aqueous solution. These strains also removed Cu and Zn from aqueous solution and were identified as Candida species. Ni uptake was efficient at pH between 4.0 and 7.0, but less efficient at pH below 3.0. The amount of Ni taken up by the yeast cells was proportional to the initial concentration of NiCl₂ below about 4 mM Ni. The cells retained the abilities to remove Ni after treatment with 10 mM EDTA or 1 M HCl for repeated usage, or after heat treatment. Received: 16 December 1996 / Received last revision: 15 April 1997 / Accepted: 20 May 1997     

Kinetics of nickel binding in hepatic and renal cytosol of63NiCl2-treated rats

Elution profiles of nickel-binding protein were investigated in hepatic and renal cytosol of rats at various time intervals (6, 16, 24, and 48 h) after intraperitoneal administration of⁶³Ni (1 mg Ni/kg. B. Wt. = 400 µCi as⁶³NiCl₂). The nickel-binding proteins were characterized in terms of absorbance at 254 nm, sulfhydryl content, and⁶³Ni counts. The results demonstrated that in liver it was bound to both high as well as low mol wt sulfhydryl proteins and glutathione-like moiety with a maximum incorporation at 16 h, after which it declined and by 48 h, very little⁶³Ni was associated with the bioligands. In kidney the incorporation of⁶³Ni was approximately 400-fold higher than liver and most of⁶³Ni was associated with the low mol. wt. sulfhydryl moiety. Kidney also exhibited maximum incorporation of⁶³Ni at 16 h that was metabolized by 48 h.     

Nickel,cobalt, and molybdenum requirement for growth of Methanobacterium thermoautotrophicum

Growth of Methanobacterium thermoautotrophicum on H₂ and CO₂ as sole energy and carbon sources was found to be dependent on Ni, Co, and Mo. At low concentrations of Ni (<100 nM), Co (<10 nM) and Mo (<10 nM) the amount of cells formed was roughly proportional to the amount of transition metal added to the medium; for the formation of 1 g cells (dry weight) approximately 150 nmol NiCl₂, 20 nmol CoCl₂ and 20 nmol Na₂MoO₄ were required. A dependence of growth on Cu, Mn, Zn, Ca, Al, and B could not be demonstrated. Conditions are described under which the bacterium grew exponentially with a doubling time of 1.8 h up to a cell density of 2 g cells (dry weight)/1.     

Coordination chemistry of 1,2-bis{di-(4-methoxyphenyl)phosphino}ethane (L-L) to nickel, palladium and platinum: Single crystal structures of [MCl2(L-L)] (M = Ni, Pd)

Square planar Ni(II), Pd(II) and Pt(II) complexes of the para-methoxy derivatised analogue of dppe, 1,2-bis{di-(4-methoxyphenyl)phosphino}ethane (L-L), [MCl₂(L-L)] and [M(L-L)₂]Cl₂ (M = Ni, Pd, Pt) are readily prepared, and have been characterised by elemental analysis, IR and NMR spectroscopies. The structures of [NiCl₂(L-L)] and [PdCl₂(L-L)] have been determined by single-crystal X-ray diffraction.     

Synthesis and characterization of square planar nickel(II) complexes with p-fluorobenzaldehyde thiosemicarbazone derivatives

New thiosemicarbazone nickel complexes (1–7), derived from p-fluorobenzaldehyde and differently substituted thiosemicarbazides, were synthetized and characterized by means of NMR and IR techniques. The p-fluorobenzaldehyde 4-ethylthiosemicarbazone Et-Hfbt (1) and its complex [Ni(Et-fbt)₂] (2) were also characterized by X-ray diffractometry. Molecule 1 consists of two units: the p-fluorobenzaldehyde residue and the thiosemicarbazonic chain. In the reaction of 1 with NiAc₂·4H₂O, complex 2 was afforded. The molecular structure of 2 consists of the neutral complexes [Ni(Et-fbt)₂] with the metal not lying on a symmetry centre, with two consequently independent ligand molecules; the coordination results in a square planar geometry slightly twisted towards a tetrahedron, involving the sulfur and the hydrazine nitrogen atoms of the two ligands in a trans configuration.     

Mechanisms of Inhibition of Pyrimidine Dimer Formation in Deoxyribonucleic Acid by Acridine Dyes

The ultraviolet (UV)-induced formation of cyclobutyl pyrimidine dimers in Escherichia coli deoxyribonucleic acid (DNA) in vitro has been investigated in terms of the mechanism of inhibition by acridine dyes, the effect on dimer yield of specific singlet and triplet quenchers, and the mechanism of dimer formation. Our results indicate that (a) energy transfer is important in dimer reduction by acridines, (b) this transfer occurs from the singlet (S₁) of DNA, and (c) at room temperature triplet quenchers do not reduce dimer yield in DNA.     

Interactive effects of gibberellin A<Subscript>3</Subscript> and ascorbic acid on lipid peroxidation and antioxidant enzyme activities in <Emphasis Type="Italic">Glycine max</Emphasis> seedlings under nickel stress

The effects of nickel in combination with ascorbic acid (AsA) and gibberellin on 7-day-old soybean seedlings were examined. Exposure to 0.25 mM NiCl₂ × 6H₂O for 5 days resulted in toxicity symptoms, such as formation of reddish-brown mottled spots on the leaf blade. Addition of 0.05 mM GA₃ or 1 mM AsA reduced toxic effects of nickel. After their simultaneous application, these symptoms did not appear. Ni decreased dry weights of roots and shoots and reduced chlorophyll content in leaves. An enhanced level of lipoxygenase activity and malondialdehyde, and changes in the activities of the antioxidant enzymes, catalase, guaiacol peroxidase and ascorbate peroxidase, in both roots and leaves indicated that Ni caused an oxidative stress in soybean plants. The Ni-stressed seedlings exposed to AsA or GA₃, especially to GA₃ plus AsA, exhibited an improved growth as compared to Ni-treated plants. GA₃ decreased Ni uptake by roots, while ascorbic acid considerably reduced root-to-shoot translocation of Ni. Interaction of AsA plus GA₃ prevented the decrease in chlorophyll content and lipid peroxidation as well as increased the activities of the antioxidant enzymes. These results suggest that GA₃ plus AsA treatment counteracts the negative effects of Ni on soybean seedlings. Published in Russian in Fiziologiya Rastenii, 2007, Vol. 54, No. 1, pp. 85–91. The text was submitted by the authors in English.     

Acorus calamus extracts and nickel chloride

Nickel, a major environmental pollutant, is known for its clastogenic, toxic, and carcinogenic potential. In this article, we report the effect of Acorus calamus on nickel chloride (NiCl₂)-induced renal oxidative stress, toxicity, and cell proliferation response in male Wistar rats. NiCl₂ (250 μmol/kg body weight/mL) enhanced reduced renal glutathione content (GSH) glutathione-S-transferase (GST), glutathione reductase (GR), lipid peroxidation (LPO), H₂O₂ generation, blood urea nitrogen (BUN), and serum creatinine with a concomitant decrease in the activity of glutathione peroxidase (GPx) (p<0.001). NiCl₂ administration also dose-dependently induced the renal ornithine decarboxylase (ODC) activity several-fold as compared to salinetreated control rats. Similarly, renal DNA synthesis, which is measured in terms of [³H] thymidine incorporation in DNA, was elevated following NiCl₂ treatment. Prophylactic treatment of rats with A. calamus (100 and 200 mg/kg body weight po) daily for 1 wk resulted in the diminution of NiCl₂-mediated damage, as evident from the downregulation of glutathione content, GST, GR, LPO, H₂O₂ generation, BUN, serum creatinine, DNA synthesis (p<0.001), and ODC activity (p<0.01) with concomitant restoration of GPx activity. These results clearly demonstrate the role of oxidative stress and its relation to renal disfunctioning and suggest a protective effect of A. calamus on NiCl₂-induced nephrotoxicity in a rat experimental model.     

Nickel dependence of factor F430 content in Methanobacterium thermoautotrophicum

Factor F₄₃₀ is a yellow compound of unknown structure present in methanogenic bacteria. It has recently been shown to contain nickel. In this communication the influence of the nickel concentration in the growth medium on the factor F₄₃₀ content of Methanobacterium thermoautotrophicum and on the nickel content of factor F₄₃₀ was studied. It was found: (1) The content of factor F₄₃₀ in the cells was strongly dependent on the nickel concentration of the growth medium. Cells grown on media with 2.5 M NiCl₂ contained 28 times as much factor F₄₃₀ per g as those grown on media with 0.075 M NiCl₂; (2) factor F₄₃₀ was synthesized in nickel deprived cells only upon the addition of nickel Nickel uptake paralleled factor F₄₃₀ synthesis; (3) independent of the nickel concentration in the growth medium, the extinction coefficient at 430 nm of factor F₄₃₀ per mol nickel was always near 22,500 cm^-1 (mol Ni)^-1. These findings indicate that nickel is an essential component of factor F₄₃₀.Dedicated to Professor Otto Kandler on the occasion of his 60th birthday