THE INFLUENCE OF METHEMOGLOBINEMIA ON THE LETHALITY OF SOME TOXIC ANIONS. I. AZIDE.
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Animals↗
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THE INFLUENCE OF METHEMOGLOBINEMIA ON THE LETHALITY OF SOME TOXIC ANIONS. II. SULFIDE.
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Animals↗
Formation and characterisation of non-toxic anionic liposomes for delivery of therapeutic agents to the pulmonary airways.
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Anions↗
Toxicity of anionic detergents determined by Saccharomyces cerevisiae microarray analysis.
Sodium n-dodecyl benzene sulfonate (LAS) and sodium dodecyl sulfate (SDS) are popular anionic detergents (surfactants) that are used worldwide and the toxicities of these chemicals have been characterized. We applied these chemicals in a DNA microarray bioassay and determined that the microarray data reflects previous findings and also provides some new information about anionic detergent toxicity. The mRNA expression profiles suggest that LAS and SDS cause damage to membranes and alterations in carbon metabolism, and induce the oxidative stress response. We also found that LAS and SDS induce the pleiotropic drug-resistance network, and that LAS and SDS may be pumped out of yeast cells by this network. Hierarchical clustering of the expression profiles showed that LAS and SDS cause similar features of toxicity and that the toxicity is similar to that of capsaicin but different from that of cadmium and mercury.
Benzenesulfonates↗
Comparative study of the acute toxicity of anionic surfactans alkyl benzene sulphonate (ABS) and sodium dodecyl sulphate (SDS) on gilthead, Sparus aurata L., eggs.
In the present work we have evaluated the acute toxicity of two anionic surfactants, alkyl benzene sulphonate (ABS) and sodium dodecyl sulphate (SDS) to eggs of gilthead Sparus aurata. At each surfactant concentration, we determined the exposure time required for 50% mortality of the eggs (LT50), surface tension and volume of oil globule in gilthead eggs. Clear dose-response relationships for mortality of gilthead eggs was observed for both toxicants; at 30 mg/L 50% mortality took place at 45 minutes for ABS and 8 minutes for SDS. At this concentration, SDS was almost six times more toxic than ABS (LT50 is compared). However, at 0.3 mg/L 50% mortality occurred after exposures of 535 minutes to ABS and 425 minutes to SDS. Descriptively, our results showed SDS was more toxic than ABS at high concentrations whereas at low concentrations their toxicity was very similar. However, statistical analysis demonstrated there were no significant differences in the toxicity of both surfactants to gilthead eggs. Surface tension value at each concentration of both surfactants was also calculated. We found that these values decreased with increasing concentration of each surfactant, and this trend was more pronounced in solutions of SDS. We also found that the volume of the oil globule of exposed eggs was influenced by surfactants. After exposure, its volume clearly decreased in comparison to controls, mainly in eggs exposed to SDS.
Animals↗
The aquatic toxicity of anionic surfactants to Daphnia magna--a comparative QSAR study of linear alkylbenzene sulphonates and ester sulphonates.
This paper develops quantitative structure activity relationships (QSARs) for the acute aquatic toxicity of the anionic surfactants linear alkylbenzene sulphonates (LAS) and ester sulphonates (ES) to Daphnia magna, the aim being to investigate the modes of action by comparing the QSARs for the two types of surfactant. The generated data for ES have been used to develop a QSAR correlating toxicity with calculated log P values: log(1/EC50)= 0.78 log P+1.37. This equation has an intercept 1.1 log units lower than a QSAR for linear alkylbenzene sulphonates (LAS). The findings suggest that either ES surfactants act by a different mode of action to LAS and other anionic surfactants or the log P calculation method introduces a systematic overestimate when applied to ES.
Alkanesulfonic Acids↗
In vitro acute toxicity of anionic surfactant linear alkylbenzene sulphonate (LAS) on the motility of gilthead (Sparus aurata L.) sperm.
This paper describes the acute toxicity of a known anionic surfactant, Linear Alkylbenzene Sulphonate (LAS), on the quality of gilthead Sparus aurata L. sperm. The parameter used to judge exposure effectiveness was sperm motility as well as its fertilizing ability after being combined with unexposed gilthead eggs. Preincubation of sperm suspensions with concentrations of LAS of 0.1, 0.5, 1, 2 and 4 mg/L caused decrease in sperm motility and fertilizing ability. In this respect, percentages of motile sperm were respectively 89.8+/-9.8, 81.7+/-16.3, 69.5+/-21.3, 57.1+/-19.1 and 21.2+/-10.9%. With regard to the percentage of fertilization success, the results were 85.7+/-8.1, 75.1+/-20.2, 62.9+/-19.7, 52.7+/-19.2 and 14.2+/-7.9% respectively. At concentrations of LAS of 0.5 mg/L or higher, the differences in both percentage of motility and fertilizing ability with controls were significant (p<5%). Although extrapolation from the laboratory to the field requires caution, the results of this work demonstrated that low-level surfactant pollution may impact directly on reproduction of the free gametes (sperm) released into water. It may lead to a long-term decline and eventual extinction of gilthead populations in nature when they are located close to effluents that are either untreated or receive inadequate secondary treatment. It is also quite important because this species constitutes an important link in the food chain and its death via exposure to surfactants may imbalance the littoral ecosystem.
Alkanesulfonic Acids↗
Acute toxicity of anionic surfactants sodium dodecyl sulphate (SDS) and linear alkylbenzene sulphonate (LAS) on the fertilizing capability of gilthead (Sparus aurata L.) sperm.
In the present work we have evaluated and compared the acute toxicity of two anionic surfactants, Sodium Dodecyl Sulphate (SDS) and Linear Alkylbenzene Sulphonate (LAS) on the fertilizing capability of gilthead Sparus aurata L. sperm. The criterion used to judge exposure effectiveness was fertilization success. Spawned eggs and sperms were collected from adult giltheads. Sperms were dosed separately with different concentrations of SDS and LAS for 60 minutes. After this period, sperms and eggs were combined for 20 minutes during which fertilization took place. Finally, the number of fertilized eggs were counted and recorded to estimate the percentage of fertilization. Exposure to SDS and LAS concentrations of 0.3, 0.6, 1.5, 3 and 6 mg/L for 60 minutes caused a significant inhibitory effect on fertilization success in gilthead Sparus aurata L.. In addition, the EC50 value for gilthead fertilization after sperm exposure was found to be 2.8 mg/L and in the case of LAS it was of 2.6 mg/L. The comparison of the results from SDS and LAS shows that the latter has a stronger negative effect on sperm viability than SDS.
Alkanesulfonic Acids↗
Oxidative stress in brain ischemia.
Brain ischemia initiates a complex cascade of metabolic events, several of which involve the generation of nitrogen and oxygen free radicals. These free radicals and related reactive chemical species mediate much of damage that occurs after transient brain ischemia, and in the penumbral region of infarcts caused by permanent ischemia. Nitric oxide, a water- and lipid-soluble free radical, is generated by the action of nitric oxide synthases. Ischemia causes a surge in nitric oxide synthase 1 (NOS 1) activity in neurons and, possibly, glia, increased NOS 3 activity in vascular endothelium, and later an increase in NOS 2 activity in a range of cells including infiltrating neutrophils and macrophages, activated microglia and astrocytes. The effects of ischemia on the activity of NOS 1, a Ca2+-dependent enzyme, are thought to be secondary to reversal of glutamate reuptake at synapses, activation of NMDA receptors, and resulting elevation of intracellular Ca2+. The up-regulation of NOS 2 activity is mediated by transcriptional inducers. In the context of brain ischemia, the activity of NOS 1 and NOS 2 is broadly deleterious, and their inhibition or inactivation is neuroprotective. However, the production of nitric oxide in blood vessels by NOS 3, which, like NOS 1, is Ca2+-dependent, causes vasodilatation and improves blood flow in the penumbral region of brain infarcts. In addition to causing the synthesis of nitric oxide, brain ischemia leads to the generation of superoxide, through the action of nitric oxide synthases, xanthine oxidase, leakage from the mitochondrial electron transport chain, and other mechanisms. Nitric oxide and superoxide are themselves highly reactive but can also combine to form a highly toxic anion, peroxynitrite. The toxicity of the free radicals and peroxynitrite results from their modification of macromolecules, especially DNA, and from the resulting induction of apoptotic and necrotic pathways. The mode of cell death that prevails probably depends on the severity and precise nature of the ischemic injury. Recent studies have emphasized the role of peroxynitrite in causing single-strand breaks in DNA, which activate the DNA repair protein poly(ADP-ribose) polymerase (PARP). This catalyzes the cleavage and thereby the consumption of NAD+, the source of energy for many vital cellular processes. Over-activation of PARP, with resulting depletion of NAD+, has been shown to make a major contribution to brain damage after transient focal ischemia in experimental animals. Neuronal accumulation of poly(ADP-ribose), the end-product of PARP activity has been demonstrated after brain ischemia in man. Several therapeutic strategies have been used to try to prevent oxidative damage and its consequences after brain ischemia in man. Although some of the drugs used in early studies were ineffective or had unacceptable side effects, other trials with antioxidant drugs have proven highly encouraging. The findings in recent animal studies are likely to lead to a range of further pharmacological strategies to limit brain injury in stroke patients.
Animals↗
[Diagnosis in metabolic acidosis of unknown origin].
BACKGROUND: Obtaining a precise diagnosis in patients presenting with metabolic acidosis of unknown origin is difficult. Poisoning with methanol or ethylene glycol should be suspected in cases with a combined increase of osmolal and anion gaps. MATERIALS AND METHODS: Retrospectively we have compared the methanol and ethylene glycol values in poisoned patients with their osmolal gaps. The anion gaps are compared to the toxic anions measured. RESULTS: There were good correlations between serum alcohols and osmolal gaps and between toxic metabolites and anion gaps. INTERPRETATION: The osmolal and the anion gaps are both helpful tools in the diagnosis of patients with metabolic acidosis of unknown origin, especially for identifying patients poisoned with methanol or ethylene glycol.
Acidosis↗
Hepatic uptake of organic anions during toxic injury by dimethylnitrosamine.
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Animals↗
Mechanisms of secretion of toxic organic anions in mammalian kidneys.
This short review considers the mechanisms of organic anion secretion in renal proximal tubules. Particular attention is given to the energy coupling of p-aminohippurate transport to inorganic anion gradients generated across both basolateral and brush-border membranes. The coupling is considered to be a consequence of the combined operation of the co-transport and anion-exchange mechanisms. A possible coexistence of several organic anion pathways with overlapping substrate specificity and/or energetic dependence of the total ion gradient are suggested. The problem of identification of transporters involved in organic anion secretion is discussed.
Animals↗
Assessment of two alternative methods for predicting the in vivo toxicities of metallic compounds.
The FRAME in vitro cytotoxicity assay and a physicochemical parameter for metal ions (i.e., "softness," sigma p) were assessed for their ability to predict the in vivo acute toxicities of 52 metallic compounds. The in vitro assay was found to be more useful, since it measures the toxicity of the whole compound, as does the in vivo method. The softness parameter applies to the metal ion only, so it cannot be used to predict the toxicity of compounds containing relatively nontoxic metal ions and toxic anions (e.g., potassium fluoride). The in vitro toxicity values (expressed as ID50 values, i.e., concentrations of test chemicals that reduced the final cellular protein content of test cultures by 50% in comparison with appropriate solvent control cultures) correlated better with mouse ip LD50 values than with rat oral LD50 values.
Animals↗
[Molecular identification of the multispecific organic anion transporter family (the OAT family): the role in the pharmacokinetics and toxicokinetics].
The multispecific organic anion transporters have been indicated to be involved in the transmembrane transport of various anionic substances. The kidney and liver possess the distinct organic anion transport pathways for the elimination of potentially toxic anionic drugs and metabolites. In the kidney, proximal tubular cells actively excrete organic anions of both endogenous and exogenous origin. We have isolated the renal multispecific organic anion transporter, OAT1 (organic anion transporter 1), from the rat kidney. OAT1 is a 551-amino acid residue protein with 12 putative membrane spanning domains. OAT1 mediates sodium-independent, anion exchange for a variety of organic anions including p-aminohippurate, cyclic nucleotides, prostanoides, dicarboxylates, and anionic drugs including beta-lactams, non-steroidal antiinflammatory drugs, diuretics and antiviral drugs. So far, three other isoforms have been identified. OATs comprise a new family of multispecific organic anion transporter, i.e., the OAT family. OATs show weak structural similarity to organic cation transporters (OCTs) and OCTN/carnitine transporters. All of the members of the OAT family are commonly expressed in the kidney, suggesting its significance in the renal organic anion excretion. In addition, OAT members appear to be responsible for the distribution/elimination of water soluble anionic drugs into/from the liver, brain and fetus.
Amino Acid Sequence↗
Sorption of Aluminum to Plasma Membrane Vesicles Isolated from Roots of Scout 66 and Atlas 66 Cultivars of Wheat.
To further elucidate the mechanisms of differential genotypic tolerance to Al, plasma membrane (PM) vesicles were isolated from whole roots, root tips, and tipless roots of Al3+-sensitive and Al3+-tolerant cultivars (cv) of wheat (Triticum aestivum L. cv Scout 66 and cv Atlas 66, respectively). Vesicles from cv Scout root tips sorbed more Al than vesicles prepared from any other source. The intrinsic surface-charge density of vesicles isolated from cv Scout was 26% more negative than vesicles from cv Atlas (-37.2 versus -29.5 millicoulombs m-2). Growth experiments indicated that cv Scout is slightly more sensitive to La3+ than is cv Atlas, that the cultivars are equally sensitive to H+, and that cv Atlas is slightly more sensitive to SeO42-. The difference in sensitivity to Al3+ was very large; for a 50% inhibition, a 16-fold greater activity of Al3+ was required for cv Atlas. Using a newly developed Gouy-Chapman-Stern model for ion sorption to the PM together with growth-response curves, we estimate that the difference in surface-charge density can account for the slightly greater sensitivity of cv Scout to cationic toxicants and the slightly greater sensitivity of cv Atlas to anionic toxicants. According to our estimates the differences in PM surface negativity and Al sorptive capacity probably account for some of the difference in sensitivity to Al3+, but the greater part of the difference probably arises from other tolerance mechanisms expressed in cv Atlas root tips that reduce the amount of Al3+ that can reach the PM.
Journal Article↗
Biophysical characterization of anionic lipoplexes.
Transfection efficiency of liposomal gene delivery vectors depends on an optimal balance in the electro-chemical and structural properties of the transfection-capable complexes. We have recently reported a novel anionic lipoplex DNA delivery system composed of a ternary complex of endogenous occurring non-toxic anionic lipids, physiological Ca2+ cations, and plasmid DNA encoding a gene of interest with high transfection efficiency and low toxicity. In this work, we investigate the electro-chemical and structural properties anionic lipoplexes and compare them with those of Ca2+-DNA complexes. Biophysical characterization is used to explain the transfection efficiency of anionic lipoplexes in mammalian CHO-K1 cells. Circular dichroism and fluorescence spectroscopy showed that the plasmid DNA underwent conformational transition from native B-DNA to Z-DNA due to compaction and condensation upon Ca2+-mediated complexation with anionic liposomes. Zeta potential measurements and gel electrophoresis studies demonstrated that Ca2+ interaction with plasmid DNA during the formation of lipoplexes also led to increased association of supercoiled plasmid DNA with the lipoplexes, leading to charge neutralization which is expected to facilitate transfection. However, even 10-fold higher concentrations of Ca2+ alone (in the absence of the anionic liposomes) were unable to induce these changes in plasmid DNA molecules. A model explaining the possible mechanism of anionic lipoplex formation and the correlation of high transfection efficiency to biophysical properties was proposed. These studies confirm the utility of biophysical studies to identify optimal formulation conditions to design efficient liposomal gene delivery vectors.
Anions↗
Dehydroabietic acid, a major anionic contaminant of pulp mill effluent, reduces both active p-aminohippurate transport and passive membrane permeability in isolated renal membranes.
The renal organic anion transport system plays a pivotal role in elimination of potentially toxic anions. This system is driven by indirect coupling to the sodium gradient at the basolateral membrane, i.e., the organic anion enters the cell in exchange for internal alpha-ketoglutarate (alpha KG) and the in greater than out alpha KG gradient is regenerated by Na+/alpha KG cotransport. The resin acid, dehydroabietic acid (DHAA), is one of several anionic xenobiotics which enter the environment secondary to pulp and paper processing. Because it is largely ionized at neutral pH (pKa, 5.7), DHAA should share the organic anion system. Indeed, Na+/glutarate-coupled p-aminohippurate (PAH) uptake by renal basolateral membrane vesicles was inhibited competitively by DHAA (Ki congruent to 150 microM). Despite the reduced rate of PAH uptake, a substantial, but delayed, overshoot was observed, suggesting additional effects. Passive permeabilities to mannitol, PAH and sodium were all decreased by DHAA, consistent with a general tightening of the membrane. Decreased permeability extended the effective lifetime of imposed ion gradients. Thus, sodium driven glutarate uptake was stimulated by 200 microM DHAA, prolonging and more than doubling its overshoot. Because the immediate driving force for PAH uptake into basolateral membrane vesicles is the magnitude of the glutarate gradient, DHAA increased the driving force for PAH uptake and permitted a substantial overshoot despite the reduced rate of PAH uptake. These data indicate that DHAA has several distinctly different effects on the membrane.
Abietanes↗
2,4-Dichlorophenoxyacetic acid intoxication increases its accumulation within the brain.
Exposure to the phenoxyacetic acid herbicides has been shown to produce neurotoxicity. Therefore, adult mice (pregnant) and rabbits were used to examine the accumulation and regional distribution of 2,4-dichlorophenoxyacetic acid (2,4-D) within the brain following intraperitoneal injection of a low dose (0.2-0.4 mg/kg) of [14C]2,4-D. Controls, i.e. animals not previously exposed to 2,4-D, were compared to animals acutely pretreated with higher doses (40-160 mg/kg) of unlabeled 2,4-D. Both autoradiography and direct tissue analysis showed that in control animals brain levels were much lower than plasma in both adult (approximately 4%) and fetus (approximately 8%). In both species, small variations were seen between the brain regions, with brainstem and cerebellum somewhat higher than other regions. Pretreatment with unlabeled 2,4-D caused a 5- to 10-fold increase in accumulation of [14C]2,4-D in both mice and rabbits. On the other hand, 2-deoxyglucose entry into the brain was not altered by 2,4-D pretreatment. Thus, there was no generalized increase in blood-brain barrier permeability. Instead, increased 2,4-D accumulation appeared to be caused by its decreased elimination from the brain. Pretreatment with 40 mg/kg led to a CSF 2,4-D concentration of 10 microM, a concentration sufficient to inhibit choroid plexus transport of [14C]2,4-D by nearly 50% in vitro. These results suggest that exposure to organic anions like 2,4-D may lead to the retention of potentially toxic anions within the CNS via competitive inhibition of the organic anion transport system which normally reduces their brain and CSF concentrations to very low levels.
2,4-Dichlorophenoxyacetic Acid↗