Silica reduces the toxicity of aluminium to a tropical freshwater fish (Mogurnda mogurnda)

The toxicity of aluminium (Al) to fish in acidic waters has been well documented. It was therefore expected that Al toxicity would be significant in fish communities in Gadjarrigamarndah (Gadji) Creek, a seasonally flowing stream in tropical northern Australia. This creek receives acidic groundwater containing elevated concentrations of Al from earlier land irrigation of treated mine tailings water from the former Nabarlek uranium mine. It was hypothesised that Al toxicity was reduced by high levels of silica (Si) in the water, and the subsequent formation of Al-silicate complexes. This prompted a laboratory assessment of the toxicity of Gadji Creek water to sac-fry of the native fish, Mogurnda mogurnda, followed by more detailed investigation of the toxicity of Al and the influence of Si in reducing Al toxicity. No mortality of M. mogurnda sac-fry was observed in two toxicity tests using Gadji Creek water collected in August 1997 and September 1998. The majority of Al (80-95%) was calculated to be complexed with humic substances and sulfate, with <1% being complexed with silicate. Assessment of the influence of silica on the acute toxicity of Al in the absence of natural organic complexants (i.e. in reconstituted freshwater, pH 5) revealed that Si reduced Al toxicity. As the molar ratio of Si:Al was increased, the percent survival of M. mogurnda sac-fry increased until there was no significant (P > 0.05) difference from the controls. However, speciation modelling again predicted that little (<3%) Al complexed with silicate, with the speciation and bioavailability of Al remaining constant as the molar ratio of Si:Al increased. Therefore, the original hypothesis that Al-silicate complexes in solution reduced the toxicity of Al to M. mogurnda could not be supported. This potential mechanism, and an alternative hypothesis, that Si competes with Al for binding sites at the fish gill surface, requires further investigation. Crown Copyright (C) 2002 Published by Elsevier Science Ltd. All rights reserved.

Chlorination for degrading saxitoxins (paralytic shellfish poisons) in water

Chlorination was investigated as a treatment option for degrading and thus removing saxitoxins (paralytic shellfish poisons, PSPs) produced by cyanobacteria (blue-green algae) from water. It was found to be effective with the order of ease of degradation of the saxitoxins being GTX5 (B1) similar to dcSTX > STX > GTX3 similar to C2 > C1 > GTX2. However the effectiveness of chlorine was pH dependent. Degradation as a function of pH was not linear with the degree of degradation increasing rapidly at around pH 7.5. At pH 9 > 90% removal was possible provided a residual of 0.5 mg l(-1) free chlorine was present after 30 min contact time. The more effective degradation at higher pH was unexpected as chlorine is known to be a weaker oxidant under these conditions. The more effective degradation, then, must be due to the toxins, which are ionisable molecules, being present in a form at higher pH which is more susceptible to oxidation. The feasibility of using chlorine to remove saxitoxins during water treatment will therefore depend strongly on the pH of the water being chlorinated. Degradation may be improved by pH adjustment but may not be a practical solution. Although saxitoxins were degraded in that the parent compounds were not detected by chemical analysis, there is no indication as to the nature of the degradation products. However, acute toxicity as determined by the mouse bioassay was eliminated.

Glutamate transporter localization does not correspond to the temporary functional recovery and late degeneration after acute ocular ischemia in rats

Purpose: To determine whether the localization of retinal glutamate transporters is affected by retinal ischaemia and whether their ability to transport glutamate decreases with the progression of ischemic retinal and optic nerve degeneration. Methods: Retinal ischemia was induced in rats by acutely increasing the intraocular pressure (IOP, 110 mmHg/60 min). Reperfusion was permitted for periods up to 60 days post-ischemia. Functional evaluation was performed by monitoring the pupil light reflexes (PLRs) and electroretinograms (flash, flicker ERG and oscillatory potentials). Glutamate transporter localization and D-aspartate (glutamate analogue) uptake were assessed by immunohistochemistry. Results: Intense immunoreactivity for the retinal glutamate transporters (GLAST, GLT1, EAAC1 and EAAT5) was observed at all time points after the insult, despite severe retinal degeneration. D-aspartate was also normally accumulated in the ischemic retinas. Ten days post-operatively the PLR ratio (ratio = indirect/direct PLR = 34 +/- 7(.)5%) was significantly less than the pre-operative value (pre-op = 76(.)7 +/- 2 (.)6%, p < 0(.)05). However, 25 and 35 days post-operatively PLR ratios did not differ significantly from pre-operative values (44(.)4 +/- 6(.)9 and 53(.)8 +/- 9(.)6%, p > 0(.)05). Forty-five and 60 days post-operatively the PLR ratio declined again and was significantly lower than the pre-operative value (33(.)8 + 8(.)7 and 26(.)2 + 8(.)9%, p < 0(.)05). Statistical analysis revealed that all tested ERG components had significantly higher values at 32, but not at 42 and 58 days post-operatively when compared to the first time point recorded post-operatively (10 days). Conclusions: While retinal glutamate transport is compromised during an acute ischemic insult, consequent retinal recovery and degeneration are not due to a change in the excitatory amino acid transporter localization or D-aspartate (glutamate analogue) uptake. Rat retina and optic nerve are capable of spontaneous, but temporary, functional recovery after an acute ischemic insult. (C) 2004 Elsevier Ltd. All rights reserved.

Nitrate-nitrate toxicity in cattle and sheep grazing Dactyloctenium radulans (button grass) in stockyards

Hungry cattle and sheep introduced to stockyards containing a dominant or pure growth of Dactyloctenium radulans (button grass) suffered acute nitrate-nitrite toxicity in four incidents in inland Queensland between 1993 and 2001. Deaths ranged from 16 to 44%. Methaemoglobinaemia was noted at necropsies in all incidents. An aqueous humour sample from one dead steer contained 75 mg nitrate/L and from one dead sheep contained 100 mg nitrate and 50 mg nitrite/L (normal = ca 5 mg nitrate/L). Both lush and dry button grass were toxic. The nitrate content of button grass from within the stockyards ranged from 4.0 to 12.9% as potassium nitrate equivalent in dry matter and from outside the stockyards ranged from

Acute cadmium chloride administration induces hepatic and renal cytochrome P450 2A5 in the mouse

Modulation of the cytochrome P450 (CYP) monooxygenase system by cadmium was investigated in male, adult DBA/2J mice treated with a single dose (16 Amol/kg body weight, i.p.) of cadmium chloride (CdCl2) at various time points. The total CYP content of kidney microsomes started to decrease 4 hours earlier than in the liver (P < 0.05), with maximal decreases at 24 hours of 56% and 85% in the liver and kidney, respectively. In contrast, both hepatic and renal coumarin 7-hydroxylase (COH) activity (indicative of CYP2A5 activity) relative to total CYP content started to progressively increase at 8 hours, with renal activity 61 times higher than the hepatic activity. Maximum increases were observed, 15-fold in the liver and 64-fold in the kidney after 24 hours. Liver and kidney CYP2A5 mRNA levels increased maximally 12 and 4 hours after treatment, respectively and decreased to almost half 6 hours later. In contrast, kidney and liver CYP2A5 protein levels increased maximally at 18 and 24 hours. This study demonstrates that hepatic and renal CYP2A5 is upregulated by cadmium with a faster response in the kidney than in the liver. This observation is concordant with the fact that kidney is the target organ for cadmium toxicity. The observed increase in the mRNA but not in protein levels after maximal induction suggests involvement of post-transcriptional mechanisms in the regulation of CYP2A5 expression by cadmium.