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Morphologic alterations in leg muscles of chicks treated with triorthocresyl phosphate in ovo
Insights
Triorthocresyl phosphate (TOCP) exposure in chick embryos caused delayed neuropathy, affecting muscle fiber size and end-plate development. Some recovery was observed, suggesting potential reinnervation in developing chicks.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Organophosphorus compounds, such as triorthocresyl phosphate (TOCP), are known to cause delayed neuropathy in adult animals.
- The effects of such compounds on the developing nervous system and musculoskeletal system are less understood.
Purpose of the Study:
- To investigate the effects of TOCP exposure on the developing myoneural apparatus in chick embryos.
- To determine if TOCP induces a delayed neuropathy in developing chicks similar to that observed in adults.
Main Methods:
- Chick embryos were injected with TOCP on incubation Day 14.
- Leg muscles (sartorius, external gastrocnemius, peroneus longus) were analyzed for muscle fiber size and end-plate length from 5 to 25 days post-hatching.
- Morphological alterations were assessed and compared to control groups.
Main Results:
- TOCP-treated chicks exhibited muscle fiber growth retardation on Day 5, followed by hypertrophy on Days 15 and 25, indicative of denervation and compensatory responses.
- Delayed end-plate development was observed on Day 15.
- These effects were more pronounced in distal leg muscles (tibial region) compared to proximal muscles (thigh).
- Partial recovery was noted by Day 25, suggesting axonal repair and reinnervation.
Conclusions:
- Developing chick embryos exposed to TOCP can develop a delayed neuropathy affecting muscle development and neuromuscular junctions.
- The observed distal effects and partial recovery support the hypothesis of TOCP-induced neuropathy in the developing chick.
- This study provides evidence that developing avian embryos may be susceptible to delayed neuropathies from organophosphorus compounds.
Abstract:
Chick embryos were injected on incubation Day 14 with 62 microliter of triorthocresyl phosphate (TOCP)/kg egg. Muscles of the leg were examined from 5 to 25 days after hatching. The sartorius from the thigh and the external gastrocnemius and peroneus longus from the tibial leg region were compared for muscle fiber size and end-plate length over this period. Treated chicks showed no acute toxic effects or overt ataxia and were equal in body weight to controls. At 5, 15, and 25 days after hatching, morphologic alterations consistent with denervation were detected. Muscle fibers were smaller than controls on Day 5 and were hypertrophic on Days 15 and 25. On Day 5 growth of fibers was retarded, an effect consistent with denervation, and the subsequent hypertrophy is predicted as compensation for denervated fibers. Small end plates were seen on Day 15, characteristic of end plates that were delayed in development by denervation. Each of these differences was greater in the tibial muscles than in the more proximally located sartorius. This is consistent with a distal neuropathy, such as that caused by TOCP in adult hens. Some recovery was apparent at the low dose 25 days after hatching. It is suggested that this resulted from reinnervation by repaired axons. This study of the myoneural apparatus and muscle fiber response to TOCP adds evidence to the possibility that the developing chick embryo may develop delayed neuropathy from organophosphorus compounds which produce this effect in adult hens.