Pearl aquaculture-profitable environmental remediation?

Bivalve molluscs are filter feeders, with pearl oysters able to filter water at rates up to 25 lh(-1)g(-1) of dry wt. tissue. Since this process leads to rapid bioaccumulation of recalcitrant pollutants such as heavy metals, organochlorine pesticides and hydrocarbons from impacted sites, it has prompted the widespread use of molluscs as biomonitors to quantify levels of marine pollution. This paper proposes pearl oyster deployment as a novel bioremediation technology for impacted sites to remove toxic contaminants, reduce nutrient loads and lower concentrations of microbial pathogens. Estimates extrapolated from the literature suggest that a modest pearl oyster farm of 100 t oyster material per year could remove 300 kg heavy metals plus 24 kg of organic contaminants via deposition into the tissue and shell. Furthermore, it was estimated that up to 19 kg of nitrogen may be removed from the coastal ecosystem per tonne of pearl oyster harvested. Pearl oysters are also likely to filter substantial amounts of sewage associated microbial pathogens from the water column. Method of cultivation and site selection are the key to minimising negative environmental impacts of bivalve cultivation. Deployment of oysters at sites with high nutrient and contaminant loadings would be advantageous, as these compounds would be removed from the ecosystem whilst generating a value-added product. Future potential may exist for harvesting bio-concentrated elements for commercial production.

Formation of dimethylarsinic acid from methylation of sodium arsenite in lumbricus terrestris.

Arsenic is ubiquitous in the environment and the toxicological response of various organisms to it is dependent on the particular chemical form involved. In general, methylation of inorganic arsenic is considered to be a detoxification reaction. While this transformation is known to be mediated by methyltransferases in several species of mammals, less is known about the fate of arsenic in invertebrates. As part of a continuing interest in heavy metals and metalloid toxicology, the alkylating activity of cytosol prepared from the common earthworm, Lumbricus terrestris, towards sodium arsenite has now been investigated. Thus, S-adenosyl-l-[(14)C]methionine ([(14)C-methyl]SAM) fortified earthworm cytosol was incubated with sodium arsenite at 37 degrees C for 90 min. Initial TLC analysis of the incubation mixture suggested incorporation of radiolabel into dimethylarsinic acid. This was subsequently proven by isolation of the metabolite through radiodilution followed by recrystallization of the recovered material to constant specific activity. This result suggests that earthworm cytosol has the same methylating reactivity towards arsenite as do similar preparations from various tissues of several species of mammals.

Ryanodyl 3-(pyridine-3-carboxylate): a novel ryanoid from Ryania insecticide.

Ryanodyl 3-(pyridine-3-carboxylate) was isolated as a minor component from the wet CHCl3 extract of Ryania insecticide, and its structure was assigned by chemical and spectroscopic methods. This compound is essentially inactive compared with ryanodine for insecticidal activity against Musca domestica adults and Tribolium castaneum larvae, for toxicity to mice, and for competition with [3H]ryanodine at the Ca(2+)-ryanodine receptor complex of skeletal muscle.

Recognition of tetramethylenedisulfotetramine and related sulfamides by the brain GABA-gated chloride channel and a cyclodiene-sensitive monoclonal antibody.

Aldrin and many other cyclodiene and polychlorocycloalkane insecticides interact with both the [35S]-tert-butylbicyclophosphorothionate ([35S]TBPS) binding site of the mammalian brain gamma-aminobutyric acid (GABA) gated chloride channel and several cyclodiene monoclonal antibodies (MAbs) at concentrations ranging from 0.06 to 8.7 microM. A survey of other classes of GABAA receptor antagonists (including picrotoxinin and several trioxabicyclooctanes) for possible interactions with the cyclodiene MAbs revealed only one potent inhibitor, the heteroadamantane tetramethylenedisulfotetramine (TETS) [mouse intraperitoneal LD50 0.24 mg/kg; TBPS binding site IC50 0.5 microM as a competitive inhibitor (Scatchard analysis); cyclodiene MAb IC50 3 microM]. These findings prompted comparative studies on the structure-activity relationships of other sulfamides as they apply to both the ligand-nerve and ligand-MAb interactions. TETS is active on only one (MAb 8H11) of four cyclodiene MAbs. Several hetero(homo)adamantanes were synthesized and compared with TETS for neurotoxicity and recognition by the TETS-sensitive cyclodiene MAb. The toxicity to mice and/or houseflies decreases in the following order: TETS much greater than the heterotetracyclic compound hexamethylenetrisulfohexamine (HEXS) and two TETS analogues in which one sulfamide group is replaced with o-phenylenediamine or 1,1-dimethyl-1,2-diaminoethane much greater than seven other hetero(homo)adamantanes. The TETS-sensitive cyclodiene MAb recognizes HEXS (IC50 0.4 microM) and, to a lesser extent, two related sulfamides. However, the cross-reactivity noted for the cyclodiene insecticides and TETS relative to the GABA-gated chloride channel (inhibition of TBPS binding) and the cyclodiene MAb does not extend to several TETS analogues including HEXS.(ABSTRACT TRUNCATED AT 250 WORDS)

Occurrence of platelet-activating factor (PAF) and an endogenous inhibitor of platelet aggregation in diffuse cutaneous mastocytosis.

We have identified PAF in the blister fluid from a patient with bullous mastocytosis, a rare form of mast-cell disease. We have found a novel endogenous inhibitor of platelet aggregation which obscured the presence of the PAF in unprocessed blister fluid and in ethanol or lipid extracts. The PAF was characterized by the demonstration of chromatographic, mass spectral and biological properties identical to those of authentic PAF. Thus this is the first demonstration of PAF in biological fluid from a patient with mastocytosis. High levels of immunoreactive prostaglandin D2 (PGD2) and histamine were also present in the blister fluid. The interaction between PAF and the inhibitor of platelet aggregation in patients with systemic mastocytosis may provide an explanation for some of the manifestations of the disease, in particular the episodic hypotension, cutaneous flushing and pallor.

Novel pyrazines from the head of Australian ponerine antRhytidoponera metallica.

The novel pyrazines, (E)- and (Z)-5-methyl-3-(2-methylbutyl)-2-(3-methylbut-1-enyl)pyrazine, (E)- and (Z)-5-methyl-3-isopentyl-2-(3-methylbut-1-enyl) pyrazine, (E)- and (Z)-5-methyl-3-(2-methylbutyl)-2-(3-methylpent-1-enyl)pyrazine, (E)- and (Z)-5-methyl-3-isopentyl-2-(3-methylpentl-enyl) pyrazine, together with the known pyrazines, 2,5-dimethyl-3-(2-methylbutyl)pyrazine and 2,5-dimethyl-3-isopentylpyrazine, have been identified from the head of the Australian ponerine antRhytidoponera metallica. Alkanes and alkenes, in small amounts, were also detected.

Probicyclophosphates: monocyclophosphates as potential prodrugs for bicyclophosphate GABA antagonists.

4-Alkylbicyclophosphates, R1C(CH2O)3P(O), with suitable R1 substituents (e.g., t-butyl, isopropyl, or cyclohexyl) are highly toxic compounds [mouse intraperitoneal (ip) LD50 values 0.036-0.52 mg/kg] and are potent noncompetitive gamma-aminobutyric acid (GABA) antagonists. 4-Alkylmonocyclophosphates of the type R1(HOCH2)C(CH2O)2P(O)R2 (where R2 is O-p-nitrophenyl, O-phenyl, S-ethyl, or S-n-propyl) are potential prodrugs by virtue of their cyclization to bicyclophosphates; thus, they may be considered as probicyclophosphates. Both the O-aryl and S-alkyl compounds cyclize via intramolecular transesterification in aqueous medium at pH 7.4 and the S-alkyl derivatives also on oxidation with m-chloroperoxybenzoic acid in chloroform and possibly with microsomal oxidases. For the isomeric O-nitrophenyl, 4-isopropyl compounds, one is equitoxic with the corresponding bicyclophosphate on ip administration to mice while the other is of very low toxicity, a result paralleled by their relative cyclization rates [k(min-1) 4 X 10(-2) and less than 4 X 10(-5), respectively]. The S-alkyl compounds are of intermediate toxicity and the O-phenyl compound is of low toxicity to mice, apparently due to less efficient conversion to the bicyclophosphates. The probable mode of action of these monocyclophosphates as potential prodrugs for bicyclophosphate GABA antagonists is further supported by receptor inhibition studies and identification of the bicyclophosphate products in enzyme systems and in the urine of treated rats.

Isolation and preliminary toxicological evaluation of arsenobetaine - the water-soluble arsenical constituent from the hepatopancreas of the western rock lobster.

The water soluble arsenic compound present in the hepatopancreas of the western rock lobster (Panulirus cygnus George) has been isolated as the reineckate salt and has been identified as arsenobetaine. Intraperitoneal injection of arsenobetaine into mice at 500 mg kg-1 did not result in mortality, and no symptoms of poisoning were observed. Mice treated with arsenobetaine at 360 mg kg-1 rapidly eliminated the compound in their excreta and no evidence was obtained for metabolic alteration. When tested in the Ames' Salmonella typhimurium system for chemical mutagens, both in the presence and absence of liver microsomal oxidase fraction, arsenobetaine gave consistently negative results.

The development of mixed function amine oxidase in cultured foetal rat hepatocytes and its relation to 3'-methyl-4-N,N-dimethylaminoazobenzene effects on tyrosine aminotransferase accumulation.

The ability of cultured foetal rat hepatocytes to metabolize the carcinogen 3'-methyl-4-dimethylaminoazobenzene (MDAB) is shown to correlate with the effectiveness of the carcinogen in suppressing the accumulation of tyrosine aminotransferase (TAT). MDAB is ineffective in cultures of 15-day gestation liver which are unable to carry out oxidation of MDAB as judged by the conversion of [3H]MDAB to a non-ether extractable form. In contrast, 19-day gestation hepatocytes can perform this function, and correspondingly the levels of TAT are suppressed in these cultures in the presence of MDAB. When 15-day gestation hepatocytes are maintained for beyond 3 days in culture, they acquire the ability to oxidize MDAB and accordingly become susceptible to the carcinogen.

The effect of carcinogens on the accumulation of tyrosine aminotransferase by foetal rat hepatocytes in culture.

The hepatocarcinogen 3'-methyl-4-dimethyl-aminoazobenzene (MDAB) suppresses the accumulation of tyrosine aminotransferase in cultured foetal hepatocytes. Experiments involving liver derived from foetuses of various ages reveals that a response is only obtained with rats older than 16-day gestation. It has been proposed that the lack of an effect in less mature hepatocytes is due to their inability to activate the carcinogen. Chemically synthesized analogues of MDAB which are considered likely to be activated forms of the procarcinogen are shown to be effective in the less mature cells. This supports the proposal that these cells may be unresponsive because they are unable to activate MDAB. Tests with other carcinogens reveal that the hepatocarcinogen dimethylbenzanthracene is also effective in 19-day gestation hepatocytes. However, the non-hepatocarcinogens azaserine and benz(a)pyrene are ineffective. Treatment with MDAB is shown not to alter the level of steroid receptor and reduce its translocation into the nucleus, suggesting that this is not the mechanism by which TAT is suppressed. The effect of the tumour promoter phorbol-myristate acetate (PMA) administered together with MDAB was shown not to modify the response to the carcinogen alone.

Delayed toxicity and delayed neurotoxicity of phosphonothioate and phosphonothioate esters.

The delayed neurotoxicity to hens and delayed toxicity to rats of the isomeric trimethyl phosphonothioates, trimethyl phosphate, and a series of the methyl and ethyl esters of methyl-, ethyl-, and phenylphosphonate and phosphonothioates were examined. All the O,O-dialkyl phosphonothioates, phosphorothioates, and their corresponding oxons were relatively nontoxic to rats, with oral LD50 values greater than the 150-450 mg/kg tested. The O,S-dialkyl phosphorothioate esters were highly acutely toxic. The rat acute LD50 values for O,S-dimethyl methylphosphonothioate and O,S-diethyl ethylphosphonothioate were 3 and 8 mg/kg. O,S-Diethyl ethylphosphonothioate and O,O, S-trimethyl phosphorothioate were the only compounds tested that showed delayed toxicity to rats. The delayed LD50 values for these two compounds were 7 and 15-20 mg/kg, respectively, with rats dying 3-22 d after treatment The delayed toxic effects were associated with continual loss of weight, reaching 18-46% at the time of death. Of this series of compounds, only O,O-diethyl phenylphosphonothioate and its oxon showed delayed neurotoxicity to hens 45 d after treatment. The minimum effective dose for these two compounds was 25 mg/kg.d administered ip for 10 d. These findings suggest that delayed neurotoxicity in hens is not due to the same mechanism as delayed toxicity in rats.

Toxicological properties of phosphorothioate and related esters present as impurities in technical organophosphorus insecticides.

O,O,S-Trimethyl phosphorothioate, an impurity in several technical organophosphorus insecticides, when administered orally to rats at single doses as low as 15 mg/kg caused delayed mortality, with death occurring 4-22 d after treatment. Delayed toxic signs were also observed in mice, but mice were generally less sensitive than rats. O,O,S-triethyl phosphorothioate and O,S,S-trimethyl phosphorodithioate induced the same signs of intoxication at slightly higher doses. Rats treated with O,O,S-trimethyl phosphorothioate refused food and water within 24 h after treatment and did not eat or drink until the time of death. Neither injection of nutrient solution nor atropine served to reduce or block intoxication. However, the isomeric O,O,O-trimethyl phosphorothioate was a potent antagonist of the toxicity of O,O,S-trimethyl phosphorothioate. As little as 1% of the O,O,O-trimethyl isomer protected rats from the intoxicating effects of the O,O,S-trimethyl isomer at doses as high as 200 mg/kg. Rat serum carboxylesterase and cholinesterase were inhibited for prolonged periods after a single oral dose of O,O,S-trimethyl phosphorothioate, but the duration of inhibition was significantly less when the toxicant contained 1% O,O,O-trimethyl isomer.

Azolla-Anabaena Relationship: VIII. Photosynthetic Characterization of the Association and Individual Partners.

Photosynthesis in the Azolla-Anabaena association was characterized with respect to photorespiration, early products of photosynthesis, and action spectra. Photorespiration as evidenced by an O(2) inhibition of photosynthesis and an O(2)-dependent CO(2) compensation concentration was found to occur in the association, and endophyte-free fronds, but not in the endophytic Anabaena. Analysis of the early products of photosynthesis indicated that both the fern and cyanobacterium fix CO(2) via the Calvin cycle. The isolated endophytic Anabaena did not release significant amounts of amino acids synthesized from recently fixed carbon. The action spectra for photosynthesis in the Azolla-Anabaena association indicated that the maximum quantum yield is between 650 and 670 nanometers, while in the endophyte the maximum is between 580 and 640 nanometers. Although the endophytic cyanobacterium is photosynthetically competent, any contribution it makes to photosynthesis in the intact association was not apparent in the action spectrum.