Impact of Ni(II), Zn(II) and Cd(II) on biogassification of potato waste.

A study was conducted on anaerobic digestion of potato waste and cattle manure mixture, inoculated with 12% inoculum and diluted to 1:1 substrate water ratio at 37 +/- 1 degrees C. Initially pH of substrate was found to be 4.5 to 5.0. Lime and sodium bicarbonate solutions were employed to adjust the pH to 7.5. Biogas production continued up to 10 and 7 days, when lime and sodium bicarbonate solutions were used to adjust the pH, respectively. Biogassification potential was studied in response to different ratio of waste and cattle manure. Biogas production rate was higher when potato waste and cattle manure were used in 50:50 ratio. Effect of two different concentrations (2.5 and 5.0 ppm) of three heavy metals viz. (Ni (II), Zn (II) and Cd (II)) on anaerobic digestion of substrate (potato waste--cattle manure, 50:50) was studied. At 2.5 ppm, all the three heavy metals increased biogas production rate over the control value. The percentage increase in biogas production over the control was highest by Cd, followed by Ni and Zn. In all the treatments, methane content of biogas increased with increase in time after feeding. Various physico-chemical parameters viz. total solids, total volatile solids, total organic carbon and chemical oxygen demand considerably declined after 7 days of digestion and decline was greater in presence of heavy metals as compared to control. The physico-chemical parameters revealed maximum decrease in the presence of 2.5-ppm concentrations of heavy metals with the substrate. Among all the three heavy metals employed in the study, Cd++ at 2.5 ppm was found to produce maximum biogas production rate. The use of three heavy metals to enhance biogas production from potato and other horticultural waste is discussed.

Biochemical responses of Camellia sinensis (L.) O. Kuntze to heavy metal stress.

Three heavy metals-mercury (II), copper (II) and nickel (II), each at a concentration of 10 and 100 micrograms/ml, were tested for their effects on various biochemical constituents of tea leaves. Both NI (II) and Hg (II) decreased the phenolic contents, while Cu (II) increased it to some extent. The metal treatments enhanced the activity of phenyl alanine ammonia lyase (PAL), while the activity of poly phenol oxidase (PPO) showed a decline. Heavy metal stress also decreased the chlorophyll content of the leaves, along with a significant reduction in Hill activity. Proline content increased significantly in all treatments.

Nickel (II)-induced apoptosis and G2/M enrichment

Treatment with certain DNA-damaging agents induce a complex cellular response comprising pertubation of cell cycle progression and/or apoptosis on proliferating mammalian cells. Our studies were focused on the cellular effects of nickel (II) acetate, DNA-damaging agent, on Chinese hamster ovary (CHO) cells. Fragmented DNAs were examined by agarose gel electrophoresis and cell cycle was determined by DNA flow cytometry using propidium iodide fluorescence. Apparent DNA laddering was observed in cells treated with 240 microM nickel (II) and increased with a concentration-dependent manner. Treatment of nickel (II) acetate resulted in apoptosis which was accompanied by G2/M cell accumulation. Proportion of CHO cells in G2/M phase was also significantly increased in cells exposed to at least 480 microM nickel (II) from 57.7% of cells in the G0/G1 phase, 34.7% in the S phase, and 7.6% in the G2/M1 phase for 0 microM nickel (II), to 58.6%, 14.5%, and 26.9% for 640 microM nickel (II). These findings suggest that nickel (II) can modulate cellular response through some common effectors involving in both apoptotic and cell cycle regulatory pathways.

Açäo do níquel nas glândulas nasais do feto de rato: estudo cariométrico / Effect of nickel on rat fetus nasal cavity glands: a karyometric study

O níquel, administrado intraperitonealmente na rata prenhe, no 10º dia de prenhez resultou em peso fetal diminuído, glândulas nasais pequenas, com núcleos mais alongados.

Tubulin aggregates induced by Ni2+ present microtubular characteristics

Rat brain tubulin in a proper buffered solution became insoluble in the presence of 10 mM NiCl2, and sedimented at centrifugal forces as low as 500 x g for 30 min. Both nickel-sedimented and microtubular tubulin conserved 65 of colchicine binding activity after 25 days of storage at -20 degrees C. However in brain cytosol, only 9 of the initial binding activity was conserved. The electrophoretic mobility of tubulin recovered from aggregates also remained unaltered. Therefore the aggregates formed with Ni2+ share important physicochemical properties with microtubules.

Effect of divalent metal ions on soluble and membrane-bound alkaline phosphatase activity in suckling rat intestine.

EDTA treatment of intestinal brush border membranes (BBM) and epithelial cell supernatant completely inhibited alkaline phosphatase (AP) activity in suckling rat intestine. AP activity was fully regained upon dialysis of the preparations against Zn2+ and to a lesser extent against Co2+, Ca2+ and Mn2+ ions. Other metal ions (Cd2+ and Mg2+) tested were essentially ineffective in restoring the enzyme activity. Considerable differences were observed in kinetic characteristics of the membrane-bound and soluble AP activities in response to various metal ions. There were apparent differences in Km, Vmax, energy of activation (Ea) and thermal stability of the soluble and membrane-bound AP activities, after metal ion substitutions. Nearly 35% AP activity was solubilized on sodium dodecyl sulphate treatment of brush borders (membrane protein: detergent ratio 1:3; w/w). Dialysis of detergent solubilized BBM against different metal ions reconstituted AP activity in the particulate fraction: the order of effectiveness was Zn greater than Ca greater than Mn greater than Co. The kinetic properties of the reconstituted AP were essentially similar to the non-integrated enzyme activity in response to various divalent metal ions examined. But there were apparent differences in Km, Vmax, Ea and thermal stability of the reconstituted AP activity compared to native brush border enzyme. The results suggest the unique requirement of Zn ions for stability and catalytic activity of the soluble and membrane-bound AP activity in suckling rat intestine.

Colchicine binding to tubulin from brain homogenates in the presence of the sugars, glycols and metal ions: effect of nickel ions on the tubulin solubility

The fact that glycerol preserves microtubules from depolymerizing in vitro, and that some ions such as Ca(II) and Mg(II), regulate the assembly-disassembly process of these structures, induced us to study the effect of several sugars, glycols and metal ions on solubility and colchicine affinity of tubulin in rat brain homogenates, and of purified microtubular protein. Inhibition of colchicine binding was significant with glycerol, polyethylene glycol 1000 (PEG-2) and the ions A1(III), Co(II), Ni(II), while compounds structurally related to glycero (glucose and sucrose) did not inhibition it. Mannitol, instead, increased the activity a 47% over control. Apparently the presence of some compounds in brain homogenates [PEG-2 (1000) and NI (II)] favored tubulin sedimentation when these latterwere centrifuged at 100,000 x g for 150 min at 20 degrees C, but the form in which tubulin becomes aggregated in the pellet is unknown. Nickel ion madeinsoluble microtubular protein of homogenates and the purified one by more than 90% without causing significant inhibition of the colchicine binding. The sediment containing nickel-treated two cycles purified microtubular protein observed with the electron microscope did not present microtubules, but it revealed the presence of irregular, wavy and streteched structures, but it revealed the presence of irregular, wavy and stretched structures bearing highly dense dotted material. The sediments became soluble in phosphate-glutamate buffer (pH 6.8) and, when incubated in polymerizing conditions, gave rise to microtubules undistinguishable from those prepared with untreated purified protein

Influence of nickel chloride on bone marrow of iron-deficient rats

Alteraçöes no peso corporal, hamoglobina, proteina sérica, ferro, fóforo e em atividades de enzizmas no soro e medula óssea foram investigadas em ratos consumindo uma dieta carente em ferro, em presença e ausencia de cloreto de niqueo (NiCl2). O grau de deficiencia em ferro, no presente trabalho foi suficiente para induzir anemia moderada, sem produzir alteraçöes nas atividade da desidrogenase-láctica total e suas isoenzimas no cérebro de ratos. Anemia moderada ocorreu somente em ratos deficientes em ferro em ausencia de cloreto de níquel. Moderada anemia ferropriva induziu elevaçäo nas actividades da desidrogenase-láctica na medula óssea, provavelmente devido a diminuiçäo na produçäo de energia através de mecanismos oxidativos. Cloreto de níquel, aparentemente por sua capacidade de alterara absorçäo de ferro e pala manutençäo do metabolismo da medula ósseas, inibiu as alteraçöes na biosíntese de hemoglobina e nas atividades da desidrogenase-láctica da medula óssea de ratos deficientes em ferro

Cloreto de níquel e aloxana: I. Determinaçäo de glicose, insulina e superóxido-dismutase em sangue e pâncreas de ratos / Nickel chloride and alloxan: I. Glucose, insulin, and superoxide dismutase determination in serum and pancreas of rats

Foi investigado o efeito do cloreto de níquel sobre a hiperglicemia induzida pela aloxana, determinando-se as concentraçöes sanguíneas de glicose e insulina, bem como o conteúdo de glicose em pâncreas e as atividades da Cu-Zn superóxido-dismutase em eritrócito e pâncreas de ratos tratados com aloxana (100 mg x Kg-1) e níquel (10 mg x Kg-1) mais aloxana. Ambas as substâncias foram adminsitradas por via subcutânea, na regiäo abdominal. Näo observamos alteraçöes significativas nas concentraçöes sanguíneas de glicose em ratos tratados com aloxana, em presença de cloreto de níquel. Ao contrário, em ausência do elemento níquel, a aloxana induziu acentuada hiperglicemia. Este efeito do níquel sobre a hiperglicemia induzida pela aloxana pode ser relacionado, a concentraçäo de insulina sérica, que foi significativamente mais elevada en presença de cloreto de níquel, em relaçäo aos animais que receberam somente aloxana. Também foi verificado que o conteúdo de glicose no pâncreas foi mais elevado, tanto nos ratos que receberam somente aloxana, como no grupo tratado com níquel e aloxana, em relaçäo aos animais controles. Parece provável que o efeito protetor do níquel a hiperglicemia induzida pela aloxana esteja relacionada a sua açäo sobre a atividade da Cu-Zn superóxido-dismutase

Efecto in vitro del cloruro de niquel sobre los mastocitos y macrofagos peritoneales / In vitro effect of nickee chloride on mastercells and peritoneal macrophages

Se investigó el efecto de diferentes concentraciones de cloruro de níquel sobre la degranulación de los mastocitos aislados de ratas y la liberación de histamina inducidos por el compuesto 48/80, así como su efecto sobre las células fagocíticas peritoneales utilizando técnicas de microscopía óptica y electrónica. El níquel no indujo la liberación de histamina de los mastocitos, en cambio sí provocó una marcada disminución de la histamina liberada por 48/80, paralelamente a un aumento en la fagocitosis de los gránulos de histamina por parte de macrófagos y eosinófilos. También indujo liberación de la enzima B galactosidasa de macrógfagos peritoneales de ratón in vitro. Se concluye que las reacciones inflamatorias por exposición al níquel no son mediadas por liberación de histamina inducida por el ión y pudieran estar relacionadas a la liberación de enzimas de los lisosomas