Introduction: It is generally recognised that zinc is an important trace element with crucial functions in cellular metabolism. The liver is responsible for zinc metabolism. Zinc deficiency can cause growth compromised effects in many organs.
Objectives: Study of the effects of zinc deficiency on the postnatal development of rat liver using histological and immunohistochemical evaluation.
Materials and Methods: Female adult rats, after matting, were allocated randomly into two groups: the control group (24 rats received a single i.p. injection of distilled water on day 9 of gestation) and the experimental group (24 rats i.p. injected 1.10 phenanthroline (zinc chelating agent) in a single dose of 30 mg/kg on day 9 of gestation). Zinc deficiency was confirmed by measuring the serum zinc level in both groups of pregnant females on the 10th day of gestation. Male offspring of treated and control rats were sacrificed at the following postnatal ages: newborn, 15 days, and three months. Samples from the liver were then processed for histological study using light and electron microscopic examination and immunohistochemical evaluation for Bcl2 expression.
Results: Light microscopic examination of the treated groups showed a disorganized hepatic architecture with apoptosis of hepatocytes. There was noticeable dilatation and congestion of blood sinusoids and central and portal vessels. Masson's trichrome stain revealed remarkable fibrosis in the treated groups' portal triad. The immunohistochemical study showed weak immunoreactivity for Bcl-2 in zinc deficient groups. The ultrastructural study showed degenerated hepatocytes with cytoplasmic vacuolations. The mitochondria appeared swollen with cristolysis and an electron-dense matrix.
Conclusion: Zinc deficiency resulted in deleterious postnatal structural effects on hepatic tissue that affected all age groups and even extended to the adult age.