A new series of some biologically active Cr(III), Fe(III), Co(II), Ni(II), Cu(II), and Zn(II) complexes was synthesized from the reaction of Ethyl 6-amino-4-(4-chlorophenyl)-5-cyano-2-methyl-4H-pyran-3-carboxylate (L) with the previous biological metals in the presence of 1,10-phenanthroline monohydrate (Phen). The structures of the obtained L along with their complexes were authenticated by different analytical and spectral techniques. The data prove that L chelates with all metal ions as bidentate through the nitrogen of the amino group and the nitrogen of the cyano group. Furthermore, Phen chelated with metal ions via two nitrogen atoms. The molar conductance values reflect that all complexes are electrolyte, confirming the 1:3 electrolytic natures for trivalent metal ions and 1:2 electrolytic for bivalent metal ions. The thermal stability and the general thermal decomposition pathways of metal complexes, L, and Phen were evaluating according to the thermogravimetric technique. The activation thermodynamic parameters were estimated from TG curves by utilizing Horowitz–Metzger (HM) and Coats–Redfern (CR) techniques. Powder X-ray diffraction (XRD) analysis proved that L, Cu(II), and Zn(II) compounds have a crystalline nature, whereas, Cr(III), Fe(III), Co(II), and Ni(II) complexes are semicrystalline. The investigated compounds were examined in vitro for their antimicrobial activity towards G(+ve) Staphylococcus aureus and Bacillus subtilis and G(−ve) Escherichia coli and Pseudomonas aeruginosa bacteria, and two fungi: Candida albicans and Aspergillus flavus. According to the findings, the Co(II) complex has a significant efficiency toward bacteria, additionally, Cr(III) complex is highly significant towards fungal strains.
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.
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