Teratogenic effects of the organophosphate insecticide, malathion, on the skeleton of developing chick embryo gross morphological study

ABSTRACT

The objective of this study was to document teratogenicity observed in chick embryos following administration of insecticide malathion in a dose of 2mg in 0.1 ml corn oil, and to suggest reasonable explanations for these anomalies. A total number of 300 eggs of Gallus domesticus species were used. After 48 hours of incubation eggs were divided into 5 groups, of 60 eggs each. The individual groups were subdivided into control [20], and treated [40] eggs. The control eggs were injected with 0.1 ml of corn oil, while the treated eggs were injected with 0.1 ml of corn oil in which 2 mg of malathion were dissolved. Eggs of both control and treated groups were examined at the 5[th], 7[th], 10[th], 14[th] and 18[th] days of incubation, for weight, mortality and morbidity, external malformations and body measurements. Embryos were prepared for skeletal examination with Alizarin red stain and Victoria blue stain. It's observed from the present study that lethality; external malformations and growth retardation, are characteristic features for malathion toxicity in chick embryo. It is observed that, malathion mortality is more frequent in higher age groups [14[th] and 18[th] days of incubation] while teratogenicity is more frequent in younger age groups [5[th] and 7[th] day of incubation]. Significant loss of weight in the treated groups is also observed. The characteristic external malformations were in the form of short lower peak, parrot beak, short neck, wry neck, micromelia of both fore limbs and hind limbs. In addition, tibiotarsal angulations and claw toes were also observed. Abnormal feather distribution, persistence of mesencephalic bulge, eye anomalies and visceral herniation could also be detected. It is concluded from this study that malathion injection is teratogenc in chick embryo when given in the 2[nd] day of incubation. The lethality detected in older age groups could be explained to be secondary to marked teratogenicity in vital organs such as heart [congestive heart failure] or neural tube defects. The toxicity of malathion on developing chick embryo could be explained by its anticholinesterase action or its suppressive effect on nicotinamid dinucleotide [NAD] levels. Also, its genotoxicity or mutagenicity could not be excluded