Newly hatched zebrafish (Brachydanio rerio) were exposed to eight compounds of selenium to establish their relative toxicities. The compounds examined included the organoselenides of methionine and cystine, the inorganic selenite salts of sodium and potassium, selenium dioxide, and the inorganic selenate salts of calcium, sodium, and potassium. The selenite compounds were more toxic to zebrafish than the selenates; the 96-h concentrations lethal to 50% of the fish ranged from 15 to 23 μg/ml for the selenites and from 81 to 82 μg/ml for potassium and sodium selenate. The limited solubility of selenocystine and the significant losses of selenomethionine from the test solutions did not allow comparable estimates to be made for the selenides. These differences in toxicity between the selenites and selenates were also demonstrated when selenium levels required to produce a 5% mortality at the end of the 10-day observation period were estimated. There was a marked difference in toxicity between the organoselenides at this level, with the toxicity of selenocystine being similar to the selenates, and selenomethionine being the most toxic of all the compounds tested.The probable role of selenium in the aquatic environment is also examined. The increasing awareness of this potentially significant pollutant, and its antagonistic nature with seven toxic or potentially toxic elements is also noted.

An optimal breeding interval of 10 days was determined for zebra fish which would insure low mortality and uniform hatching among replicate samples. Egg mortality increased from 5% to 100% as the time interval between breeding periods was increased from 10 days to 40 days. Most larvae hatched 5 days after fertilization, although hatching was influenced by the time interval between breeding periods. Egg production differed among individuals of the same replicate to a greater extent than the influence of time between breeding intervals.

Malathion is one of the organophosphorous insecticides least toxic to mammals. The toxicity of this compound in chick embryos is known; however, its teratogenic nature has not been recorded. Concentrations of 3.99 and 6.42 milligrams of malathion were injected into the yolk sacs of 4- and 5-day-old incubated eggs respectively. This procedure consistently produced deformed chicks with a combination of sparse plumage, micromelia, overall growth retardation, and beak defects.

Embryos at four stages of development and the newly hatched larvae of zebrafish (Brachydanio rerio) were exposed to selenium concentrations between 0.5 and 10 μg/ml to establish the toxic levels at the different stages. Embryo mortality was negligible at all selenium concentrations. Following hatching, mortality among the larvae sharply increased at concentrations of 3 μg/ml or greater irrespective of the embryonic stage when exposed. For most treatments, over 90% of the larvae died within 10 days of hatching. The mortality rate for larvae exposed to selenium after hatching was slightly less.

Malathion-induced teratisms in the chick embryo included hind limb, beak, and feather defects as well as overall growth retardation. Various metabolites were injected along with malathion into fertile eggs in an attempt to determine the possible effect of the latter compound on metabolism. Of those compounds injected tryptophan prevented both the malformations and the growth retardation while nicotinamide, nicotinic acid, and quinolinic acid prevented the malformations only. Other compounds related to tryptophan by electronic reactivity enhanced the effect of malathion. A cholinesterase assay on embryo homogenates revealed no relationship between cholinesterase levels and teratisms.

Organophosphate poisoning in fish and mammals has always been associated with the inhibition of acetylcholinesterase in both neuromuscular and brain tissues. This inhibition resulted in the apparent death of the organisms by asphyxia. Rarely have other effects been reported.In the present study, 1-inch rainbow trout larvae were treated for 16 hr with from 10 to 100 ppm Dylox, or for 40 hr with 5 ppm. This treatment produced a marked acetylcholinesterase inhibition that was reflected by their abnormal behaviour patterns. Histological examination revealed pathological changes in the heart, liver, blood cells, pseudogills, and muscular tissues; this pathology could not be explained on the basis of acetylcholinesterase inhibition.

Etsd-plates in the thigh muscles of duck embryos were first recognized with mynistoylcholine as substrate at thse 19th day of incubation. Each appeared as a cholinesterase-positive dot sunrounded by a snsall halo which rapidly increased in size during the 20th and 21st days. The endplates were unsually oval in shape, averaging 33 X 25 z with a subneunral apparatus 5-12

The organophosphate Malathion produces malformations in the limbs of chick embryos. Staining with buffered toluidine blue reveals abnormal areas in the cartilage characterized by hypertrophy of the chondroblasts, lack of ground substance, and weak (gamma) γ metachromasia. Radioautography with S35 shows little incorporation into the chondroitin sulfates of the cartilage ground substance.