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Effect of selenium and mercury on gross morphology and histopathology of chick embryos
Insights
Selenium and mercury toxicity in chick embryos cause distinct developmental defects and organ damage. Combined exposure results in combined toxic effects, particularly in the kidneys.
Area of Science:
- Toxicology
- Developmental Biology
- Comparative Pathology
Background:
- Selenium and mercury are environmental toxicants with known teratogenic potential.
- Understanding the specific effects of these metals on embryonic development is crucial for risk assessment.
Purpose of the Study:
- To investigate the teratogenic and histopathological effects of selenium and mercury exposure in chick embryos.
- To compare the individual and combined toxicological impacts of selenium and mercury.
Main Methods:
- Chick embryos were exposed to selenium (selenite) and mercury (chloride) at different developmental stages.
- Gross lesions and histopathological changes in the liver and kidneys were examined.
Main Results:
- Selenium exposure caused limb defects, beak malformations, gastroschisis, and specific liver and kidney lesions.
- Mercury exposure induced leg defects and distinct liver and kidney pathologies, including degeneration.
- Combined exposure showed mercury-like liver effects but retained some selenium-induced kidney damage.
Conclusions:
- Both selenium and mercury exhibit significant teratogenic and organotoxic effects in developing chick embryos.
- Combined exposure leads to a complex pattern of toxicity, with some overlapping and some distinct pathological findings.
Abstract:
Gross lesions of selenium toxicity in chick embryos included webbed, fused, and curled toes; cracked, crooked, and shortened beaks and gastroschisis. Mercury injection on day 3 of incubation caused leg defects but older embryos were much less susceptible. Histopathological studies showed that injection of selenium as selenite caused dissociation of hepatic cells, particularly around the central veins. Glomeruli of affected kidneys were enlarged, and in each glomerulus the lumen of the capillary tuft was dilated and the space of Bowman widened. Epithelial cells of the proximal convoluted tubules were detached from the basement membranes. Injection of mercury as chloride resulted in liver pathology in the late dead embryos which included dilated central veins and sinusoids. The cytoplasm of many hepatic cells was vacuolated. Foci of hemorrhages were observed in all liver lobes. In the kidneys, the renal corpuscles showed either shrinkage or enlargement. They seemed to be in the process of degeneration and disintegration. Sclerotic glomeruli were characterized by disappearance of Bowman's space and clumping of the glomerular tuft. Combined treatment with selenium and mercury resulted in liver pathology similar to that observed in mercury toxicity. The hepatic cell dissociation seen in selenium treated embryos was not observed following the combined treatment. In the kidneys the combined treatment resulted in typical lesions of both selenium and mercury toxicity.