Removal of iron from groundwater by ash: a systematic study of a traditional method.

A traditional method for removal of iron from ground water by using ash has been systematically investigated. Ashes from five different sources, viz., banana rind, banana pseudostem, banana leaf, rice husk and bamboo has been studied. The principle applied is enhanced precipitation of iron at high pH caused by ash. The study included laboratory analysis of some relevant chemical parameters of the ashes and the efficiency of the ashes in removing iron from prefabricated water with respect to quantity of ash and corresponding increase in pH of water. The ash of banana pseudostem has been found to be most suitable for removal of iron. A low-cost and easily made iron removal system for household use has been designed and tested in the laboratory. The ash of banana pseudostem has been found to remove iron to below 0.3ppm without increasing the pH above the acceptable limit. The optimum values of the different parameters for removal of iron are 200-300mgl(-1) ash, 1.0lh(-1) flow rate and 1h of contact time with ash for groundwater having [Fe] of about 2.20ppm. The amount of ash can be increased for groundwater having higher [Fe] and can be decreased gradually during continuous use of the system. Acceptability of the method has been examined based on chemical analysis of the treated water. Increase in the essential minerals such as Ca, K has been observed in the water after treatment. The designed iron removing system is expected to be suitable for household use.

Acute toxicity and cardio-respiratory effects of 2-deoxy-D-glucose: a promising radio sensitiser.

OBJECTIVE: To evaluate the acute toxicity of 2-deoxy-D-glucose (2DG) by oral (p.o.) and intravenous (i.v.) routes, and also the cardio-respiratory effects following high doses of 2DG in animal models. METHODS: The LD50 of 2DG (in water) was determined in rats and mice by p.o. route and in mice by i.v. route. The effect of 2-DG (250 mg/kg, 500 mg/kg, and 1000 mg/kg, i.v.) was studied on various cardio-respiratory parameters viz., mean arterial blood pressure, heart rate and respiratory rate in anaesthetised rats. The effect of 2DG (500 mg/kg, 1000 mg/kg, and 2000 mg/kg, p.o.) was also studied on various respiratory parameters viz., respiratory rate and tidal volume in conscious rats and mice using a computer program. RESULTS: The p.o. LD50 of 2DG was found to be >8000 mg/kg in mice and rats, and at this dose no death was observed. The LD50 in mice by i.v. route was found to be 8000 mg/kg. At this dose 2 out of 4 mice died and the death occurred within 6 h. A significant increase in the body weight was observed after p.o. administration of 2DG in rats at 500 mg/kg, 1000 mg/kg, and 2000 mg/kg doses. There was no significant change in the body weight at 4000 mg/kg and 8000 mg/kg by the p.o. route in rats and up to 8000 mg/kg by p.o. as well as i.v. routes in mice. Intravenous administration of 2DG (250 mg/kg, 500 mg/kg, and 1000 mg/kg) in anaesthetised rats showed a time-dependent decrease in the mean arterial blood pressure. There was no change in the heart rate in any of the treatment groups. The tidal volume was not changed significantly by p.o administration in conscious rats, but a significant decrease in the respiratory frequency at 500 mg/kg and 1000 mg/kg doses was observed. In the mice also there was no change in the tidal volume after p.o, administration, but the respiratory frequency decreased significantly at 2000 mg/kg dose. CONCLUSION: 2DG is a safe compound but can cause a fall in the blood pressure and a decrease in respiratory frequency at high doses.

Haematological, hepatic and renal alterations after repeated oral or intraperitoneal administration of monoisoamyl DMSA. I. Changes in male rats.

Monoisoamyl 2,3-dimercaptosuccinic acid (MiADMSA), a vicinal thiol chelator, is gaining recognition recently as a better chelator than meso 2,3-dimercaptosuccinic acid (DMSA) in decreasing heavy metal burden in tissues because of its lipophilic character. There is, however, little information available on the toxicological properties of this chelator after repeated administration in animals. In the present study, we investigated the dose-dependent effect of MiADMSA on various biochemical parameters suggestive of alterations in haem biosynthesis and hepatic, renal and brain oxidative stress after 21 days of repeated intraperitoneal (i.p.) or oral (p.o.) administration to rats. The concentration of essential metals in blood and soft tissues was determined along with histopathological observations of hepatic and renal tissues. The results suggest that MiADMSA administration had no effect on blood delta-aminolevulinic acid dehydratase activity. However, an increase in zinc protoporphyrin and a decrease in haemoglobin levels were noted in animals given MiADMSA i.p. A moderate increase in serum alkaline phosphatase suggested mild hepatotoxicity at the highest dose (100 mg kg(-1), i.p.). This was confirmed by histopathological examinations, which identified basophilic stippling, granulation of the cytoplasm, haemorrhage and congestion. At the highest dose, levels of hepatic thiobarbituric acid reactive substance and oxidized glutathione were increased above those of control values. Levels of hepatic reduced glutathione were decreased. Taken together, these observations point to oxidative stress. In animals administered MiADMSA i.p. there was an increase in the brain malondialdehyde levels at the two higher doses (50 and 100 mg kg(-1)). Essential metal status revealed a significant effect of MiADMSA (p.o.) in increasing blood zinc while significantly decreasing the kidney zinc level. The most significant adverse effect of MiADMSA was on copper concentration, which showed significant depletion from almost all major organs. Magnesium levels in blood decreased but increased in liver of MiADMSA-administered rats. Histopathological observations of liver and kidneys suggest few moderate lesions. It can be concluded that repeated administration of MiADMSA is compromised with some mild toxic effect, particularly the loss of copper. The effects during oral administration are comparatively less pronounced than by the i.p. route.

Relative potency of synthetic analogs of Ptychodiscus brevis toxin in depressing synaptic transmission evoked in neonatal rat spinal cord in vitro.

Effects of Ptychodiscus brevis toxin (PbTx) analogs on the spinal synaptic transmission in neonatal rats in vitro were evaluated. PbTx1/PbTx2 had aromatic groups and PbTx3/PbTx4 had aliphatic groups. All the analogs depressed monosynaptic reflex (MSR) and polysynaptic reflex (PSR) in a concentration-dependent manner. The maximal depression of MSR (75% from initial) and PSR (96%) was at 84 microM for PbTx1. Concentration to produce 25% inhibition from initial (IC25) by PbTx1 for MSR and PSR was < or =2.8 microM. The maximal depression of MSR (80%) was at 96 microM and PSR (100%) was at 32 microM by PbTx2. IC25 for MSR and PSR were 5.5 microM and <3.2 microM, respectively. PbTx3 decreased MSR by 25% maximally (=IC25) at 36 microM. The depression of PSR fluctuated and was maximal (75%) at 108 microM and IC25 was 6.2 microM. PbTx4 depressed MSR and PSR at the maximum of 35% at 32 microM and IC25 for MSR was 8.3 microM and for PSR was 35 microM. Rank order of potency of toxins for depressing MSR was PbTx1>PbTx2>>PbTx4>PbTx3; and for PSR it was PbTx2>PbTx1>PbTx3>>PbTx4. Results indicate that the toxins having aromatic groups exhibited greater neurotoxicity.

Toxic effects of arsenic (III) on some hematopoietic and central nervous system variables in rats and guinea pigs.

OBJECTIVE: To evaluate the effects of arsenic (III) exposure on porphyrin metabolism and the central nervous system supplemented with data on the effect of hepatic and renal tissues of rats and guinea pigs. METHODS: Rats and guinea pigs were exposed to 10 or 25 ppm arsenic in drinking water for 16 weeks. RESULTS: Following chronic arsenic (III) exposure, delta-aminolevulinic acid dehydratase activity in blood showed a significant reduction as did the total cell counts (RBC and WBC) and reduced glutathione with increased urinary delta-aminolevulinic acid. Zinc protoporphyrin, a sensitive indicator of iron deficiency and impairment of heme biosynthesis, showed a significant increase in arsenic exposure. The hepatic delta-aminolevulinic acid dehydratase and delta-aminolevulinic acid synthetase activity increased in chronic arsenic (III) exposure in rats and guinea pigs. Significant changes in the steady-state level of three major neurotransmitters, dopamine, norepinephrine, and 5-hydroxytryptamine, and monoamine oxidase were observed following chronic arsenic (III) exposure. CONCLUSION: At low doses (10 and 25 ppm in drinking water), the effects of arsenic on hematopoietic indices and whole-brain neurotransmitter concentrations were more prominent in guinea pigs than in rats with some variability in the dose response.

Antidotal efficacy of pyridinium oximes and cholineacetyltransferase inhibitors against organophosphorus intoxication in rodents.

In an attempt to develop effective antidote against organophosphorus intoxication, some new imidazole-pyridinium mono-oximes, long chain pyridinium mono-oximes and cholineacetyltransferase inhibitors were synthesised. These compounds were evaluated for their in vivo therapeutic protection and neuromuscular function studies in rodents. The results indicate that SPK-series oximes may be useful against sarin poisoning without any beneficial effect against VX (O-Ethyl S-2-NN-diisopropylaminoethyl methylphosphonofluoridate) intoxication. The cholineacetyltransferase (ChAT) inhibitors may not be of any help against any of the OP compounds studied in this study.

Dose response of sulphur mustard: behavioral and toxic signs in rats.

The present study elucidates the behavioral and toxic signs in rats following dermal application of sulphur mustard (SM). Graded doses of SM (0.10, 0.25, 0.50, 0.75 and 1.0 LD50) were topically applied to male Wister rats. The body weight as well as behavioral/toxic signs and symptoms were recorded at 1, 2, 3, and 4th day after application of SM. Sulphur mustard consistently decreased body weights of rats in a dose and time dependent manner with maximum decrease on 3rd day post treatment. Sedation and diarrhea were significant in response to doses of SM intoxication in rats. It is concluded that the body weight, sedation and diarrhea may be used as a reliable parameter in evaluating SM intoxication. It is also suggested that hydration and hypertonic saline must be used as a rescue agent within 1-3 days after exposure to SM.

Changes in certain hematological and physiological variables following single gallium arsenide exposure in rats.

Gallium arsenide (GaAs), a group III-VA intermetallic semiconductor, possesses superior electronic and optical properties and has a wide application in electronic industry. Exposure to GaAs in the semiconductor industries could be a possible occupational risk. The aim of the present study was to determine the dose-dependent effect of single oral exposure to GaAs (500, 1000, or 2000 mg/kg) on some biochemical variables in heme synthesis pathway and few selected physiological variables at d 1, 7, and 15 following administration. The results indicate that GaAs produced a significant effect on the activity of delta-aminolevulinic acid dehydratase (ALAD) in blood and heart (particularly at d 7) following exposure to 2000 mg/kg, whereas urinary delta-aminolevulinic acid (ALA) excretion was elevated only at d 7. No marked influence of GaAs on blood hemoglobin, zinc protoporphyrin, and packed cell volume was noticed. Blood glutathione (GSH) was significantly reduced at d 7, but remained unchanged at two other time intervals. On the other hand, heart GSH contents remained uninfluenced on GaAs exposure. Most of the physiological variables, viz. blood pressure, heart and respiration rate, and twitch response, remained unchanged, except for some minor alterations observed at d 7 and 15 following exposure to GaAs at a dose of 2000 mg/kg. Blood gallium concentration was not detectable in normal animals and rats exposed to 500 mg/kg GaAs. Blood arsenic concentration was, however, detectable even at the a lower dose level and increased in a dose-dependent manner. All these changes showed a recovery pattern at d 21, indicating that the alterations are reversible.

Calcium modulatory properties of O,O-diphenyl O-N-cyclooctyl phosphoramidate [corrected] isolated from Ptychodiscus brevis in rat atria and smooth muscle.

Calcium modulatory activity of a marine toxin has been studied employing in vitro preparations. The toxin induced contracture in rat diaphragm was not modified by denervation, d-tubocurarine and tetrodotoxin (TTX). In contrast, varying concentrations of calcium, EGTA and ryanodine inhibited the contracture significantly. The toxin produced a series of repeating contractions in vas deferens. Experiments with TTX, adrenoceptor blockers and other agents exclude a release of neuromediators or direct stimulation of post synaptic receptors to account for the rhythmic effect in vas deferens. The dependence of rhythmicity on external Ca2+ concentration and inhibiting effect of Mn2+, ryanodine and nifedipine indicate a direct activation of voltage-sensitive calcium channel. The toxin also evoked a similar pattern of response in paced atria mediated through Ca2+ influx.

Mechanism of cardiotoxicity induced by a marine toxin isolated from Ptychodiscus brevis.

An organophosphate toxin of marine origin isolated from red tide dinoflagellate P. brevis produced a dose-dependent dual effect on rat atria, i.e. positive inotropic effect at low concentrations (2.8 x 10(-8) to 8.4 x 10(-7) M) and negative inotropic and chronotropic responses at an elevated dose (4.8 x 10(-6) to 7.2 x 10(-4) M). The negative chronotropic and inotropic responses of the toxin were potentiated with physostigmine and ouabain whereas antagonized by atropine and hemicholinium-3 pretreatments and those effects remained unaltered by isoproterenol, phenylephrine and ouabain pretreatments. The results indicate that the toxin induced negative inotropic and chronotropic effects are mediated through release of acetylcholine from the nerve endings and consequent activation of muscarinic receptor. In atria exposed to guanethidine, bretylium, propranolol and tyramine tachyphylaxis, the positive inotropic response of the toxin was not modified. However, the response was antagonized by EGTA, nifedipine, ryanodine, calcium-free ringer and potentiated with caffeine and amiloride pretreatments. The results suggest that the positive inotropic effect of the toxin is mediated through Ca2+ influx and impairment of Na+/Ca2+ exchange process.

Cardiovascular effects of an organophosphate toxin isolated from Ptychodiscus brevis.

The dose-dependent hypotensive and bradycardic effects induced by an ichthyotoxic organophosphate compound isolated from the marine dinoflagellate Ptychodiscus brevis were studied. These effects were not antagonized by atropine, but potentiated by alpha-adrenoceptor blocker and hexamethonium. The toxin abolished the vasopressor effect elicited by phenylephrine, indicating an alpha-adrenergic blocking activity. The cardiovascular depressor responses were antagonized by tetraethylammonium while blockade of cholinergic and histaminergic receptors or inhibition of prostaglandin synthesis failed to modify these effects. The results indicate that the cardiovascular depressor effects of the toxin are probably mediated through alpha-adrenergic and ganglionic blockade accompanied by modulation of potassium channel activity.

Diisopropylphosphorofluoridate-induced depression of compound action potential of frog sciatic nerve in vitro is mediated through the inhibition of cholinesterase activity.

Effect of diisopropylphosphorofluoridate (DFP), an irreversible cholinesterase (ChE) inhibitor, on compound action potential (CAP) of sciatic nerve in vitro was examined. Further, the role of cholinesterase reactivator (1 acetyl-4-hydroxy imino methyl pyridinium bromide; SPK-3) in reversing DFP-induced changes was also evaluated. Diisopropylphosphorofluoridate produced a dose-dependent depression of the CAP. A concentration as low as 0.01 microM DFP produced a 5% depression (P < 0.05) and the maximal depression (30% of control) was observed with 1 microM. The SPK-3 (up to 10 microM) had no effect on the CAP; SPK-3 (10 microM) antagonized the DFP-induced depression of the CAP partially but not after 1 microM DFP. However, the inhibitory concentration of DFP to produce 50% of the maximal depression (IC50) was 0.38 +/- 0.025 microM in the presence of SPK-3 (10 microM; n = 4), against 0.15 +/- 0.05 microM for DFP alone (n = 7). These IC50 values were significantly different (P < 0.05, Student's t-test). The DFP decreased nerve ChE activity by 41% in the absence of SPK-3 and by 31% in the presence of SPK-3. Although SPK-3 could not completely reactivate the inhibited enzyme, it seems reasonable to conclude that the DFP-induced depression of the action potential of sciatic nerve was mediated by inhibiting the ChE activity.

Effect of topically applied sulphur mustard on antioxidant enzymes in blood cells and body tissues of rats.

The effect of sulphur mustard (0.5 LD50, percutaneous) on antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)) in blood cells (erythrocytes (RBC), leucocytes (WBC) and platelets) and body tissues (liver, kidney, spleen and brain) of rats has been investigated 24 h post exposure. The SOD activity was significantly decreased in WBC, platelets, spleen and brain as compared to control. The CAT activity was significantly inhibited in RBC, WBC and spleen as compared to control. The GSH-Px activity was signficantly depressed in WBC, spleen and liver as compared to control. It is concluded that sulphur mustard at a sublethal dose inhibited antioxidant enzyme activities in WBC and spleen. Thus, antioxidant enzymes in lymphatic tissues may be used as suitable models for assessing mustard toxicity. The study suggests the formation of reactive oxygen species in sulphur mustard intoxication.

Liver slice culture for assessing hepatotoxicity of freshwater cyanobacteria.

1. A modified mouse liver slice culture technique was established and the viability of the system was assessed on the basis of leakage of cytosolic enzymes viz. lactate dehydrogenase (LDH), alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartic aminotransferase (AST) and slice histology. 2. This system was employed for toxicity screening of five algal species of Indian origin on the basis of the EC50 for LDH leakage (dose of cyanobacteria resulting in leakage of 50% of enzyme) of a known toxic cyanobacterial strain Microcystis aeruginosa (PCC 7820). On the basis of both in vitro and in vivo toxicity none of the five species screened exhibited toxicity. 3. The toxicity of PCC 7820 was compared with a purified cyanobacterial hepatotoxin, Microcystin-LR. Various biochemical indices and histological changes confirm the hepatotoxic nature of the toxins. 4. The toxins did not induce glutathione-mediated lipid peroxidation but they did cause significant mitochondrial damage based on an MTT assay. 5. The study illustrates the utility of this in vitro system in identifying naturally occurring toxic cyanobacteria, particularly hepatotoxic species.

Cardiovascular and respiratory changes following exposure to a synthetic toxin of Ptychodiscus brevis.

The present study demonstrated cardiorespiratory effects of a synthetic phosphorus-containing ichthyotoxic metabolite elaborated by the marine dinoflagellate Ptychodiscus brevis in anaesthetised cats. The metabolite at a dose of 0.25-1.5 mg/kg i.v., resulted in a dose-dependent fall in blood pressure and such vasodepressor effect was associated with bradycardia. There is initial respiratory apnoea followed by increased rate and depth of respiration (hyperapnoea) following the administration of the toxin. The hypotensive response was accompanied by a decrease in aortic baroreceptor activity. The ECG showed atrioventricular conduction block, arrhythmia and depression of S-T segment and T wave which indicated coronary insufficiency. Vasodepressive property of the toxin is presumably muscarinic in nature as atropine counteracted the vasodepression.

Toxicity evaluation of two treatment regimens for cyanide poisoning.

Toxicological evaluation of two recently reported treatment protocols for cyanide--SN (sodium nitrite) + DMAP (4-dimethylaminophenol) and SN + HA (hydroxylamine)--was carried out in male rats. Both treatments produced transient hyperammonaemia and decreased mean arterial pressure. Heart rate decreased and respiratory rate increased, but these changes reached the level of significance only after SN + HA. Histopathological lesions in lung, liver (SN+HA) and kidney (SN+DMAP) were predominantly in the vicinity of blood vessels. The results indicate toxic effects in both treatment groups at a dose known to induce methaemoglobin concentration to the level of antidotal efficiency in cyanide intoxication.

Therapeutic potential of meso 2,3-dimercaptosuccinic acid or 2,3-dimercaptopropane 1-sulfonate in chronic arsenic intoxication in rats.

The therapeutic efficacy of two thiol chelators, meso 2,3-dimercaptosuccinic acid (DMSA) or 2,3-dimercaptopropane sulfonate (DMPS) in treating chronic arsenic intoxication was investigated in male rats. Both the chelators were effective in promoting urinary arsenic excretion and restoring arsenic induced inhibition of blood delta-aminolevulinic acid dehydratase activity and hepatic glutathione level. Elevation of urinary delta-aminolevulinic acid excretion and arsenic concentration in blood, liver and kidneys were reduced significantly by both the chelators. Histopathological lesions induced by arsenic were also effectively reduced by the above chelators. DMSA being more effective than DMPS. The results suggest DMSA and DMPS to be effective antidotes for treating chronic arsenic toxicity in experimental animals.

Concurrent acute exercise alters central and peripheral responses to physostigmine.

This study reports the modulatory effects of physostigmine (Phy) and concurrent acute exercise on the time course of cholinesterase (ChE) activity, the rate of decarbamylation (Kd), and half-time of recovery of ChE in red blood cells (RBC) and various tissues of rats. Acute exercise equivalent to 80% VO2-max (maximal oxygen consumption) transiently increased the RBC ChE activity, whereas Phy decreased ChE activity in RBC and various tissues. Physostigmine along with concurrent acute exercise increased the Kd in RBC, brain, and heart by 56.4%, 66.7%, and 139%, respectively, compared to Phy alone. The Kd in diaphragm and muscle decreased to 14.1% and 56.2%, respectively, compared to Phy alone. The variation in Kd might be due to the effect of concurrent acute exercise on the redistribution of Phy in various tissues of rat as a result of changes in blood flow.