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A pesticide store near Hargeisa (Somaliland) was damaged by bombing in May 1988, and subsequently looted by local people, who removed and drained drums of chemicals. Assessment of the effects of resultant spillage during the dry season, March/April 1993, established that pesticides, mainly organochlorines (dieldrin and products and BHC isomers)and organophosphates (fenitrothion and malathion) had contaminated 3700 sq mof soil at up to 3728.0 (geometric mean 149.0) ppm (5180.0 g/m3)total insecticides. Reptiles avoided contamination above 1 ppm, and were absent above 10 ppm. Experimental contact with highly contaminated soil caused death in lizards-Hemidactylus parkeri and Mabuyas. striata-after 26.5 and 33. 5 h, respectively (residue levels elevated over 2000-and 149-fold), and 100% mortality within 65 min in frogs Tomopterna cryptotis (geometric mean residue level elevated 168-fold). Sediment 350 m downstream of the spill contained dieldrin at 0.50 ppm (0.03-0.05 ppm after 1.6, to 9.0, km). Whole body residues of spillage vicinity lizards were up to 1.52 ppm wet weight (193.6 ppm lipid) total insecticides. Geometric mean of 0.36 ppm was elevated fivefold above mean background level of Hargeisa lizards in the valley below. Dieldrin and products was highest; the level of BHC isomers was also significantly higher than DDT. Geometric mean total insecticide level in Chalcides ragazzii and H. parkeri was four times higher than in surface-dwelling Pseuderemias smithi. Reptile species richness was habitat-influenced. Frogs without abnormalities present in mud of river-bed wells indicated uncontaminated ground water (organochlorine residues undetected). Low levels in frogs, and of M. s. striata in thevicinity of wells [geometric means 0.09 and 0.07 (ranges 0-0.48 and 0.01-0.31) ppm, respectively], implied that by 2.7 km downstream of the spill few residues were entering food chains.

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The impact of DDT ground-spraying against tsetse flies on lizards was investigated in NW Zimbabwe. Nineteen species were recorded, 17 in mopane woodland and 11 on gritstone outcrops: Mabuya striata wahlbergii dominated trees and Mabuya quinquetaeniata margaritifer rocks. Mean frequency of M. s. wahlbergii declined significantly from 76% of lizards at untreated sites (n = 8), through 72% after three annual treatments (n = 4), to 48% after 4-6 treatments (n = 6). Sighting rates and proportion of trees occupied were also significantly lower at treated than untreated sites. Numbers on trunks (99% > 15 cm diameter) above 3 m increased significantly with years of treatment relative to those in the spray target area below 3 m. Total DDT loads rose significantly with number of annual treatments and were up to 263 microg g(-1) lipid (7 microg g(-1) wet body weight) after 3-6 years. The percentage of unaltered DDT increased with load, which was proportionately higher in thin than in fat lizards. The geometric mean total DDT level in M. s. wahlbergii was significantly higher than in outcrop species, and from treated woodland was elevated 21 times above that in lizards from treated outcrops. Frequency and sighting rates of Lygodactylus chobiensis in woodland and immature Agama kirkii on outcrops were significantly higher in treated than in untreated areas.

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Investigations to determine dermal contamination of rural farmers during pesticide application to tropical crops are described. Contamination patterns and levels vary according to crop type and height, and application method. Non-toxic model pesticides and tracer dyes were applied to rice, vegetable, mango, cotton and coffee crops in the Philippines, Thailand, Tanzania and Malawi, using knapsack and ULV spinning disc sprayers. Tracer dye falling on the operator during application was measured for each type of crop sprayed. Mean gross dermal deposits of dye were: rice 97 mg/hr; mango 257 mg/hr; vegetables 103 mg/hr; cotton 220 mg/hr; coffee 95 mg/hr. The implications of these gross dermal deposit figures in relation to pesticide contamination and hazard are discussed.

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The degradation and short-term resynthesis of adenine nucleotides have been examined in a preparation of isolated rat heart myocytes. These myocyte preparations are essentially free of vascular and endothelial cells, contain levels of adenine nucleotides quite comparable to those of intact heart tissue, and retain these components remarkably well for up to 2 h of aerobic incubation in the presence of 1 mM Ca2+. When the cells are rapidly and synchronously de-energized by addition of uncoupler, an inhibitor of respiration and iodoacetate, cellular ATP is degraded almost quantitatively to AMP. The AMP is then converted to either intracellular adenosine, which accumulates to high concentrations before release to the cell exterior, or to IMP. The relative contribution of these two pathways depends on the metabolic state of the cells just prior to de-energization, with IMP production favored when respiring cells are de-energized and adenosine formation predominant when glycolyzing myocytes are subjected to this treatment. Cells de-energized by anaerobiosis in the absence of glucose lose ATP and adenine nucleotides with the production of IMP and adenosine. Upon reoxygenation, these cells restore a high adenylate energy charge and about 60% of control levels of GTP. There is a net resynthesis of 5-7 nmol of adenine nucleotides.mg-1 protein with a corresponding decline in IMP. Added [14C]adenosine labels the adenine nucleotide pool, but little net resynthesis of adenine nucleotides via adenosine kinase can be detected. It therefore appears that a rapid regeneration of adenine nucleotides can occur via the enzymes of the purine nucleotide cycle in heart myocytes and is limited by the size of the IMP pool retained.

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Oxaloacetate keto-enol tautomerase, partially purified from porcine kidney, catalyzes the conversion of enol- to keto-oxaloacetate by a mechanism in which solvent protons end up equally distributed between the two prochiral positions at C3 of keto-oxaloacetate. This conclusion is based upon the observation that when enzyme catalyzed ketonization is conducted in 3H2O in the presence of excess malate dehydrogenase and NADH, only 50% of the 3H in the isolated (2S)-[3-3H]malate is labilized to solvent upon treatment with fumarase. From a stereochemical perspective, this enzyme is unlike phenylpyruvate keto-enol tautomerase that is known to catalyze stereospecific proton transfer between solvent and the pro-R position of keto-substrate. As a result of an attempt to clarify the physiological importance of oxaloacetate tautomerase activity, keto-oxaloacetate was demonstrated to be directly transported across the inner membrane of rat liver mitochondria on the basis of the results of kinetic and isotope-trapping experiments.

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The Ca2+ sensitivity of a population of isolated adult rat heart myocytes has been related to the Na+ content of the cells prior to Ca2+ exposure, and the intracellular free Ca2+ as reported by quin2 fluorescence when the cells are challenged with millimolar external Ca2+. Myocytes exposed to Ca2+ during quin2 loading show a resting intracellular free Ca2+ of 150 +/- 30 nM and retain the rod cell morphology of heart cells in situ. The myocytes take up Na+ and lose K+ when incubated in the cold in the absence of Ca2+. Large numbers of these rod-shaped, Na+-loaded myocytes hypercontract into grossly distorted round cell forms when exposed to physiological levels of Ca2+. The number of cells that hypercontract is proportional to the Na+ content of the cells prior to Ca2+ addition and can be directly related to the intracellular free Ca2+ concentration attained following Ca2+ addition. Fifty percent of the cells in a myocyte population hypercontract when the internal free Ca2+ concentration reported by quin2 reaches 400 nM and virtually all of the cells hypercontract when this value reaches 1 microM. The entry of Ca2+ into Na+-loaded myocytes is biphasic with one phase inhibited by Ca2+ channel blockade. This suggests that Ca2+ enters Na+-loaded myocytes by the Ca2+ channel as well as by Na+/Ca2+ exchange.

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