Treatment of acute cobalt intoxication in rats with L-methionine

The antidotal action of L-methionine in acute cobalt (II) chloride intoxication given orally or intraperitoneally to rats has been investigated in this paper. The doses of CoCl2 (2.73 mmole/kg oral, 0.21 mmole/kg i.p.) are always above their LD50 for both means of administration, reaching during oral administration values above its LD95 (4.20 mmole/kg). The doses of L-methionine varied from 0.63 mmole/kg (i.p.) to 8.19 mmole/kg (orally). L-methionine did not show a significant antidotal action (mortality rates) against the other sulphurous aminoacid: L-cysteine, which is considered an effective antidote. The administration of Co2+-methionine chelates prepared in vitro, showed rates of 10% mortality when given orally and 30% when given intraperitoneally, against Co2+-cysteine and co2+-N-acetylcysteine chelates with rates of 0% mortality. No significant functional changes were observed in the survivors killed seven days after administration in groups receiving L-methionine. Although L-methionine cannot be considered an effective antidote, it is likely to reduce partially the toxic effects of cobalt.     

Amorphous MoS3 Infiltrated with Carbon Nanotubes as an Advanced Anode Material of Sodium‐Ion Batteries with Large Gravimetric,Areal, and Volumetric Capacities

The search for earth‐abundant and high‐performance electrode materials for sodium‐ion batteries represents an important challenge to current battery research. 2D transition metal dichalcogenides, particularly MoS₂, have attracted increasing attention recently, but few of them so far have been able to meet expectations. In this study, it is demonstrated that another phase of molybdenum sulfide—amorphous chain‐like MoS₃—can be a better choice as the anode material of sodium‐ion batteries. Highly compact MoS₃ particles infiltrated with carbon nanotubes are prepared via the facile acid precipitation method in ethylene glycol. Compared to crystalline MoS₂, the resultant amorphous MoS₃ not only exhibits impressive gravimetric performance—featuring excellent specific capacity (≈615 mA h g^?1), rate capability (235 mA h g^?1 at 20 A g^?1), and cycling stability but also shows exceptional volumetric capacity of ≈1000 mA h cm^?3 and an areal capacity of >6.0 mA h cm^?2 at very high areal loadings of active materials (up to 12 mg cm^?2). The experimental results are supported by density functional theory simulations showing that the 1D chains of MoS₃ can facilitate the adsorption and diffusion of Na⁺ ions. At last, it is demonstrated that the MoS₃ anode can be paired with an Na₃V₂(PO₄)₃ cathode to afford full cells with great capacity and cycling performance.     

Lack of stimulation of renal (Na+ + K+)-ATPase by thyroid hormones in the rabbit

The effect of l-3,5,3′-triiodothyronine (T₃) and thyroxine (T₄) on (Na⁺ + K⁺)-ATPase activities was examined in rabbit kidneys because in this tissue almost 80% of the metabolism is connected to active sodium transport. T₃-receptor concentrations were estimated as 0.62 and 0.80 pmol/mg per DNA in the cortex and outer medulla, respectively. A dose of 0.5 mg T₃/kg body weight for 3 days increased basal metabolic rate by almost 60%, and the mitochondrial 1-α-glycerophosphate dehydrogenase activity was increased by 50% in both the cortex and medulla. (Na⁺ + K⁺)-ATPase activity in the liver was raised by almost 50%. However, no changes in (Na⁺ + K⁺)-ATPase activities or binding sites for [³H]ouabain in either the kidney cortex or medulla could be observed. T₄ at 16 mg/kg daily for 14 days was also without effect on renal (Na⁺ + K⁺)-ATPase activities. Furthermore, the response to T₃ was absent at high sodium excretion rates induced by unilateral nephrectomy and extracellular volume expansion. Thus, despite stimulation of basal metabolic rate and renal 1-α-glycerophosphate dehydrogenase activity by T₃ and T₄, the (Na⁺ + K⁺)-ATPase activity in the rabbit kidney is identical in euthyroid and hyperthyroid states. However, thyroid hormones prevent the normal natriuretic response to extracellular volume expansion.     

Prevention by sodium 4,5-dihydroxybenzene1,3-disulfonate (tiron) of vanadium-induced behavioral toxicity in rats

Recent studies have shown that oral vanadate (V⁵⁺) administration results in behavioral toxicity in rats. The chelating agent Tiron (sodium 4,5-dihydroxybenzene-l,3-disulfonate) is an effective antidote in the removal of vanadium from vanadium-loaded rats. In this study, the protective activity of Tiron on vanadate-induced behavioral toxicity was evaluated in adult rats. Intraperitoneal treatment with Tiron at 235 or 470 mg/kg was initiated after 6 wk of oral sodium metavanadate administration (16 mg/kg/d) and continued for 2 wk. Although vanadate exposure did not result in a significant reduction in the general activity of the animals in an open field, a lower active avoidance acquisition could be observed. However, the vanadate-induced behavioral deficit was reverted by Tiron administration at 470 mg/kg. The present results suggest that Tiron may protect, at least in part, against metavanadate-induced behavioral toxicity.     

The chemistry of rhenium and technetium. Part III. The synthesis and characterisation of oxo-bis-(tetrathiomolybdenato)-technetium(V) and its reduction by triphenylphosphine

The Complexes (Bu₄N)[TcO(MoS₄)₂] and Tc- (PPh₃)₂(MoS₄)₂ were prepared. The former complex has a much lower Tc-O stretching frequency than is generally found gor the TcO³⁺. moiety. The latter technetium(IV) Complex was obtained by the reduction of Tc^(v) O(MoS₄)₂^? with triphenylphosphine and also by the substitution reaction of TcCl₄(PPh₃)2 with MoS₄^2-. Previous reductions of this nature have led to the isolation of species that differ by two formal oxidation state numbers from the oxidant.     

Dealkylation of pentoxyresorufin: A rapid and sensitive assay for measuring induction of cytochrome(s) P-450 by phenobarbital and other xenobiotics in the rat

The O-dealkylation of pentoxyresorufin (7-pentoxyphenoxazone) by rat liver microsomes was examined. The reaction appeared highly specific for certain phenobarbital inducible forms of cytochrome P-450 and was increased 95- to 140-fold by animal pretreatment with phenobarbital (75 mg/kg/day, four ip injections) and ~50-fold by Aroclor 1254 (500 mg/kg, one ip injection) while animal pretreatment with 3-methylcholanthrene (50 mg/kg/day, three ip injections) resulted in less than a 2-fold increase over the rate detected in control microsomes. It was observed that this activity, in microsomes for Aroclor-pretreated rats, was dependent on O₂ and was inhibited by metyrapone and SKF 525-A, indicative of cytochrome(s) P-450 mediation in the reaction. When antibodies directed against purified cytochrome(s) P-450S were employed to inhibit the pentoxyresorufin O-dealkylation reaction, antibodies to P-450_PB-B greatly inhibited the reaction (>90%), while antibodies to P-450_PB-C or P-450_PB/PCN-E had minimal effects. Assay of hepatic microsomes from rats which were pretreated with varying doses of phenobarbital (0.9–75 mg/kg/day, four ip injections) indicated that while aminopyrine-N-demethylase activity was induced only 2-fold at the maximum dose (75 mg/kg/day), pentoxyresorufin O-dealkylase activity was induced ~140-fold at this dose and ~4-fold by a dose of phenobarbital as low as 0.9 mg/kg.     

Effects of phenoxide ligation: Synthesis and characterization of the [Mo2Fe6S8(SEt)3(OPh)6]3− ion

Reaction of phenol with an alkylthiolate-ligated double cubane complex effects phenolate substitution at the terminal positions; the product can be isolated as its benzyltriethylammonium salt. The phenolate cluster possesses unaltered magnetic properties and blue shifted optical spectra, and undergoes ligand exchange reactions with electrophiles as expected for terminal phenolate substitution. Increased isotropic proton NMR shifts and large negative shifts in corresponding first and second reduction potentials are consistent with increased donation of electron density to the [MoFe₃S₄]³⁺ cores for phenolate versus thiophenolate terminal ligands to iron. Similar behavior has been observed for Fe₄S₄, Fe₂S₂ and MoS₂Fe systems.     

Computer simulation for effect of Pr(III) on Ca(II) speciation in human interstitial fluid

A multiphase model of metal ion speciation in human interstitial fluid was constructed and the effect of Pr(III) on Ca(II) speciation was studied. Results show that free Ca²⁺, [Ca(HCO₃)], and [Ca(Lac)] are the main species of Ca(II). Because of the competition of Pr(III) for ligands with Ca(II), the percentages of free Ca²⁺, [Ca(Lac)], and [Ca(His)(Thr)H₃] increase gradually and the percentages of CaHPO₄(aq) and [Ca(Cit)(His)H₂] decrease gradually with the increase in the total concentration of Pr(III). However, the percentages of [Ca(HCO₃)] and CaCO₃(aq) first increase and then begin to decrease when the total concentration of Pr(III) exceeds 6.070×10⁻⁴ M.     

Computer simulation for effect of Pr(III) on Ca(II) speciation in human interstitial fluid

A mutiphase model of metal ion speciation in human interstitial fluid was constructed and the effect of Pr(III) on Ca(II) speciation was studied. Results show that Ca(II) mainly distributes in free Ca²⁺, [Ca(HCO₃)], and [Ca(Lac)]. Because of the competition of Pr(III) for ligands with Ca(II), with the total concentration of Pr(III) rising, the percentages of free Ca²⁺, [Ca(Lac)] and [Ca(His)(Thr)H₃], gradually increase and the percentages of CaHPO₄(aq) and [Ca(Cit)(His)H₂] gradually decrease. However, the percentages of [Ca(HCO₃)] and CaCO₃(aq) first increase, and then begin to decrease when the total concentration of Pr(III) exceeds 6.070×10⁻⁴ M.     

Response of red-osier dogwood (Cornus stolonifera) seedlings to sodium sulphate salinity: effects of supplemental calcium

A greenhouse study was designed to test the effects of sodium sulphate (Na₂SO₄) on red-osier dogwood (Cornus stolonifera Michx) seedlings in the presence and absence of additional calcium (Ca²⁺). Changes in growth parameters, ion and carbohydrate accumulation and cell wall composition were examined. Calcium alleviated the effect of Na₂SO₄ on shoot height; however, it did not affect the reduction in shoot and root dry weights. An increased level of sodium (Na⁺) in roots of plant exposed to Na₂SO₄ was recorded in the presence of supplemental Ca²⁺ whereas there was no change in potassium (K⁺) and Ca²⁺ levels. In shoots of seedlings treated with Na₂SO₄, the addition of Ca²⁺ did not affect Na⁺, K⁺ and Ca²⁺ levels. The amount of soluble carbohydrates was increased in leaves of seedlings treated with Na₂SO₄ both in the absence and presence of supplemental Ca²⁺. The decrease in cell wall material in response to salt stress was alleviated by Ca²⁺ in stem tissues although Ca²⁺ did not alter the changes in hemicellulose and cellulose. Sugar composition of pectins and hemicellulose were modified in stems and leaves by Na₂SO₄ and/or Ca²⁺. The results of this study showed that calcium was able to alleviate the effects of salt stress on shoot height and cell wall content of red-osier dogwood stems. Furthermore, changes occurred in cell wall composition of red osier seedlings treated with Na₂SO₄.     

Comparison of the effectiveness of 2,3-dimercaptopropanol (BAL) andmeso-2,3-dimercaptosuccinic acid (DMSA) as protective agents against mercuric chloride-induced nephrotoxicity in rats

The effectiveness of 2,3-dimercaptopropanol (BAL) andmeso-2,3-dimercaptosuccinic acid (DMSA) on HgCl₂-induced nephrotoxicity was studied in the rat. Seven groups of adult male rats were given a single sc toxic dose of HgCl₂ (0.68 mg/kg) followed by 0.9% saline (positive control group), BAL (15, 30, and 60 mg/kg) or DMSA (50, 100, and 200 mg/kg) administered ip at 0, 24, 48, and 72 h thereafter. Although the renal function of HgCl₂-exposed rats was slightly improved after BAL administration, Hg concentrations in the kidney were only reduced at 60 mg/kg. In addition, the protective effect of BAL was not dose-related. In contrast to BAL, DMSA was effective in increasing the urinary excretion of Hg and in reducing the renal Hg content. These results show that DMSA would be more effective than BAL in preventing or in protecting against inorganic Hg-induced nephrotoxicity.     

Protective effect of omega-3 fatty acid against mercury chloride intoxication in mice

The aim of this study was to investigate the protective effect of omega-3 fatty acid in HgCI₂ toxicity in mice. Levels of malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NO) and total sialic acid (TSA), and histopathological changes in selected organs were evaluated. Twenty-eight mice were equally divided into 4 groups, namely Groups I–IV. Group I animals received intraperitoneal (ip) injection of physiological saline solution; Group II animals received ip injection of 0.4 mg/kg/day HgCI₂; Group III animals received ip injection of 0.4 mg/kg/day HgCI₂ in addition to subcutaneous (sc) injection of 0.5 g/kg/day omega-3 fatty acid; and Group IV animals received sc injection of 0.5 g/kg/day omega-3 fatty acid. All treatments lasted 7 days. The levels of MDA, NO and TSA were significantly higher in Group II and lower in Groups III and IV as compared to the Group I. GSH level was the highest in Group IV. In histopathology, severe degeneration in liver and kidney was observed in Group II animals. These degrading changes were seen to be reduced greatly in Group III animals. The results suggested that omega-3 fatty acid might attenuate HgCI₂-induced toxicity by improving antioxidant status and acute phase response in mice.     

Copper and molybdenum absorption by rats given ammonium tetrathiomolybdate

Previous studies have shown that the tetrathiomolybdate ion [MoS_4^2?] is a potent antagonist of Cu metabolism. Effects of orally administered MoS_4^2? on the absorption and tissue distribution of ⁶⁴Cu in rats have now been investigated. Four or 12 mg Mo/kg diet, when given as MoS_4^2?, strongly inhibited ⁶⁴Cu absorption and modified the fate of absorbed Cu, decreasing hepatic and renal uptake but increasing plasma retention of ⁶⁴Cu. These effects were not induced by equivalent dietary concentrations of Mo as MoS_4^2? or when S^2? was given as CaS. Clinical and biochemical effects induced by orally administered MoS_4^2? were abolished by increasing dietary concentrations of Cu. Such treatment also inhibited the absorption and tissue retention of ⁹⁹Mo derived from ⁹⁹MoS_4^2?. Intraperitoneal administration of Cu ameliorated clinical effects attributable to MoS_4^2? but neither inhibited ⁹⁹Mo absorption nor the appearance of systemic defects in Cu metabolism. Since the absorption of MoS_4^2? (or its derivatives) from the gastrointestinal tract is inhibited by Cu, it is evident that the site of its action as an antagonist influencing either the absorption or the subsequent metabolic fate of Cu depends upon the ratio Cu/MoS_4^2? in the diet.     

Hepatoprotective effects of phosphatidylserine liposomes on carbon tetrachloride-induced hepatotoxicity in rats

It has been proposed carbon tetrachloride (CCl₄) intoxication due to the production of free radicals and serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) overload results hepatotoxicity. Phosphatidylserine (PS) has shown antioxidant activity in numerous studies. Therefore, this study was aimed to investigate the effects of PS liposomes treatment against the CCl₄-induced hepatotoxicity in a rat model. Male Wistar rats were treated with PS (10 mg/kg, oral) or phosphatidylcholine liposomes (PC) (10 mg/kg, oral) for 3 days before CCl₄ (2 ml/kg; ip once on the third day) injection. The serum level of ALT, AST, and ALP were measured. Also, antioxidant assays were performed. Administration of PS with CCl₄ significantly inhibited alterations in the serum levels of AST, ALP (^**P < 0.01), and ALT (^***P < 0.001) compared with control group. Furthermore, measurement of malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) levels indicated that PS significantly reduced reactive oxygen species. The results of the present study showed the hepatoprotective effects of PS against CCl₄-induced hepatotoxicity in rats.     

Fructokinase (Fraction III) of Pea Seeds

A second fructokinase (EC 2.7.1.4) was obtained from pea seed (Pisum sativum L. var. Progress No. 9) extracts. The enzyme, termed fructokinase (fraction III), was specific for fructose and had little activity with glucose. With fructose concentrations above 0.25 millimolar, there was strong substrate inhibition at the optimum pH (8.0) and also at pH 6.6. The apparent K_m values at pH 8.0 for fructose and glucose were 0.06 millimolar and 0.14 millimolar, respectively. The apparent K_m for Mg adenosine 5′-triphosphate (MgATP) was 0.06 millimolar and excess MgATP was inhibitory. Mg²⁺ was essential for activity but the enzyme was inhibited by excess Mg²⁺ or ATP. Mg adenosine 5′-pyrophosphate was also inhibitory. Activity was stimulated by the addition of monovalent cations: of those tested K⁺, Rb⁺, and NH₄⁺ were the most effective. The possible role of fructokinase (fraction III) is discussed.     

THE BIOLOGICAL ACT'IVITIES OF YELLOW AZALEA,RHODODENDRON MOLLE G. DON AGAINST THE VEGETABLE LEAFMINER,LIRIOMYZA SATIVAE (DIPTERA: AGROMYZIDAE) *

Abstract The results of laboratory and greenhouse bioassays indicated that Rhodojaponin‐ III (Abbr. R‐ 1) and extracts of flowers from Rhododendron molle G. Don possessed signficant feeding inhibition and insectcidal properties against the larvae and adults of Liromyzia sativae. Treated with 500 mg/L R‐ III 1 000 mg/L molosul‐tap, and 10 000 mg/L methanol(MeOH) ethyl acetate (EtOAc), CH₂Cl₂, methanol‐water (MeOH‐H₂O) extracts the rates of feeding inhibition were 77. 34 % 74.30 % 82.15 % 77.50 % 67. 33 % 62.85 % against the 2nd instar larvae, and were 67.66% 55.21 % 49.72% 54.26% 46.81 % 38.53% against the 3rd instar larvae, respectively;LC₅₀ values against the 2nd instar larvae were 208.65, 166.05, 2.74 ± 10³,766.72, 5.95 ± 10³, 1.85 ± 10³mg/L, and against 3rd larvae were 300.62, 256.00, 4.33 ±10³, 1.03 ± 10³,9.79 ± 10³, and 2.62± 10³mg/L, respectively. Against the adults, LC₅₀ values of R‐III EtOAc extract and molosultap were 159.07.723.87 and 134.55mgL respectively after treatment for 24 h.     

Histological Changes in Kidney and Liver of Rats Due to Gold (III) Compound [Au(en)Cl2]Cl

Introduction

Development of novel metallodrugs with enhanced anti-proliferative potential and reduced toxicity has become the prime focus of the evolving medicinal chemistry. In this regards, gold (III) complexes with various ligands are being extensively investigated. In the current study renal and hepatic toxicity of a newly developed gold (III) compound [Au(en)Cl₂]Cl was assessed by histopathological evaluation of liver and kidney specimens of rats exposed to the compound.

Methods

Male rats (n = 42) weighing 200–250 gram were injected single, varying doses of gold (III) compound [(dichlorido(ethylenediamine)aurate((III)]chloride [Au(en)Cl₂]Cl in the acute toxicity component of the study. In the sub-acute toxicity part, a dose of 32.2 mg/kg (equivalent to 1/10 of LD50) was administered intraperitoneally for 14 consecutive days before sacrificing the animals. After autopsy, the renal and hepatic tissues were preserved in buffered formalin. Processing of the samples was followed by histopathological evaluation. The results were compared with the normal controls (n = 11).

Results

A dose of 32.2 mg/kg (1/10 of LD₅₀) revealed no renal tubular necrosis. The predominant histopathological finding was mild pyelitis, a prominence of eosinophils and mild congestion. The hepatic lesions comprised varying extents of ballooning degeneration with accompanying congestion and focal portal inflammation.

Conclusion

Gold (III) compound [Au(en)Cl₂]Cl causes minimal histological changes in kidney and liver of rats, reflecting its relative safety as compared to other clinically established antineoplastic drugs.     

Comparison of tin and lead toxic action on erythropoietic system in blood and bone marrow of rabbits

The aim of this work was to assess and compare morphological changes in blood and bone marrow of rabbits afterper os (po) or intraperitoneal (ip) administration of equimolar doses of tin or lead. The experiment was performed on female rabbits that were divided into four groups of six animals each, and received stannous chloride SnCl₂×2 H₂O (Merck) or lead acetate Pb(CH₃COO)₂ (POCh Gliwice) in equimolar doses (ip—17/uM/kg) orper os (po—85/uM/kg). Group I was administered SnCl₂ ip at the dose of 2 mg Sn/kg every day for 3 mo, group II Pb(CH₃COO)₂ ip at a dose of 3.5 mg Pb/kg every day for 3 wk, group III po SnCl₂ (10 mg Sn/kg), and group IV po Pb(CH₃COO)₂ (17.5 mg Pb/kg), both for 4 mo. The morphological factors hemoglobin (Hb), hematocrit (Ht), erythrocyte (Ercs), and reticulocyte counts, MCV, MCH, MCHC, and erythropoietic system in bone marrow aspirates with sideroblast count, iron concentration, TIBC, and SI were estimated. Tin caused hemolytic anemia depending on abnormal iron utilization. After ip administration of tin, anemia was observed during the whole time of the study, whereas after po exposure, transient anemia was noticed. It has been proven that the mechanism of toxic action of tin on hematopoietic system is similar to the toxic effect of lead.     

Evaluation of the Acute Oral Toxicity Class of Trinuclear Chromium(III) Glycinate Complex in Rat

Chromium(III) is considered as an essential element playing a role in carbohydrate and lipid metabolism, and various chemical forms of this element are widely used in dietary supplements. A new trinuclear chromium(III) glycinate complex [Cr₃O(NH₂CH₂CO₂)₆(H₂O)₃]⁺NO₃⁻ (CrGly), an analogue of Cr3 (trinuclear Cr(III) propionate complex) has been synthesized as a potential source of supplementary Cr. In this study, we evaluated the acute toxicity class of CrGly in Wistar rats applying the OECD 423 procedure. Male and female Wistar rats (n = 12, 6 ♀ and 6 ♂) were given by gavage either a single dose of CrGly 2,000 mg/kg body mass (equals to 300 mg Cr(III)/kg body mass; in aqueous solution) or equivalent volumes of distilled water and fed ad libitum commercial Labofeed B diet, and observed carefully for 14 days, then sacrificed to collect blood and internal organs for biochemical and histologic examination. No death cases were detected. No abnormalities in animal behavior, body mass gains, gross organ histology, or blood morphology and biochemistry were observed. The results demonstrate that LD₅₀ of CrGly is greater than 2,000 mg/kg when administrated orally to rat; thus, this compound appears to belong to the fifth category in the GHS system or the fourth class (“unclassified”) in the EU classification system.