Copper is a trace element and has a vital role in homeostasis but it has cumulative effects and may be hazardous to the animal, human, and environment. Copper is a vital trace element to all living as it participates in various metabolic processes and is controlled via complicated homeostatic mechanisms, but excess copper has a deleterious effect in organisms as it stimulates free radical production in the living cell, lipid peroxidation, and disturbs the whole-body antioxidant capacity. Although its beneficial effect, it has a hazardous effect on health as it has genotoxic, developmental toxicity, and hepatic toxicity in experimental animals

Objective: To evaluate the postnatal toxicity of copper oxychloride (COC) in lactating female albino rats. Design: Randomized controlled experimental study. Animals: Eighteen pregnant female albino rats weight 150±10 g and 6-7 week old. Procedures: Eighteen pregnant female albino rats were divided into 3 groups treated orally with copper oxychloride 0, 73.5, 147 mg/kg (equivalent 1/20 and 1/10 of LD50) daily from first day of parturition for 21 days. Female rats and its offspring were euthanized at 21 days of treatment. The postnatal toxic effect in the neonates and dams were estimated through biochemical biomarkers as metabolic and oxidative stress biomarkers, histopathological and hematological evaluation. Results: There was a significant increase in liver enzymes activities as ALT and GGT and oxidative stress biomarker as MDA (P < 0.05) in both suckling pups and lactating dams beside decrease the level of metabolic biomarkers as glucose, total protein and cholesterol (P < 0.05). Additionally, antioxidant enzymes as SOD and CTA (P < 0.05) were reduced significantly in the treated groups in a dose dependent manner in comparison to control group. Moreover the histopathological revealed that Dams treated with COC at both doses shown degenerative changes and intralobular histiocytic infiltration with intralobular fibroblastic proliferation in the hepatic tissue. Neuronal necrosis, neuronophagia and astrocytosis in the brain tissue with degenerative changes of purkinje cells in cerebellum. Fibrous tissue proliferation of renal glomeruli with degenerative changes in renal tubular epithelium and marked lymphoid depletion in the splenic tissue in dose dependent manner. While Suckling pups of treated dams with different doses of COC shown focal histiocytic and lymphocytic infiltration besides congestion of portal vein and margination of leukocytes, focal edema in the neuropils with focal hemorrhagic areas in the brain tissue, degeneration in the renal glomeruli and severe lymphoid depletion with congestion of the splenic sinusoids in dose dependent manner. Conclusion and clinical relevance: The potential postnatal toxic effect of copper oxychloride in neonates and lactating female albino rats through transmammary transmission in milk clarified from biochemical and histopathological evaluation of dams and its pups.

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To evaluate the postnatal toxicity of copper oxychloride (COC) in lactating female albino rats. Design: Random iz e d controlle d experim e ntal study. Animals : Eightee n pregna nt female albino rats weight 150±10 g and 6-7 week old. Procedures: Eighteen pregnant female albino rats were divided into 3 groups treated orally with copper oxychloride 0, 73.5, 147 mg/kg (equivalent 1/20 and 1/10 of LD50) daily from first day of parturition for 21 days. Female rats and its offspring were euthanized at 21 days of treatment. The postnatal toxic effect in the neonates and dams were estimated through biochemical biomarkers as metabolic and oxidative stress biomarke rs, histopa thological and hematological evaluation. Results: There was a significant increase in liver enzymes activities as ALT and GGT and oxidative stress biomarker as MDA (P < 0.05) in both suckling pups and lactating dams beside decrease the level of metabolic biomarkers as glucose, total protein and cholesterol (P < 0.05). Additionally, antioxidant enzymes as SOD and CTA (P < 0.05) were reduced significantly in the treated groups in a dose dependent manner in comparison to control group.Moreover the histopathological revealed that Dams treated with COC at both doses shown degenerative changes and intralobular histiocytic infiltration with intralobular fibroblastic proliferation in the hepatic tissue. Neuronal necrosis, neuronophagia and astrocytosis in the brain tissue with degenerative changes of purkinje cells in cerebellum. Fibrous tissue proliferation of renal glomeruli with degenerative changes in renal tubular epithelium and marked lymphoid depletion in the splenic tissue in dose dependent manner. While Suckling pups of treated dams with different doses of COC shown focal histiocytic and lymphocytic infiltration besides congestion of portal vein and margination of leukocytes, focal edema in the neuropils with focal hemorrhagic areas in the brain tissue, degeneration in the renal glomeruli and severe lymphoid depletion with congestion of the splenic sinusoids in dose depende nt manner. Conclusion and clinical relevance:The potential postnatal toxic effect of copper oxychloride in neonates and lactating female albino rats through transmammary transmission in milk clarified from biochemical and histopathological evaluation of dams and its pups.