Scholarlink

<p>The present study aims to evaluate the hematotoxicity and renal toxicity of cobalt iodide nanoplates (CoI<sub>2</sub> NPs) in albino mice, validated through pharmacokinetic and molecular docking analyses. CoI<sub>2</sub> NPs were synthesized and characterized for morphology, crystalline structure, and functional groups using scanning electron microscopy (SEM), X-ray diffraction (XRD), and Fourier transform infrared spectroscopy (FTIR), respectively. Albino mice were divided into control and treatment groups (low dose 2.27&#xa0;mg/kg, high dose 4.55&#xa0;mg/kg CoI<sub>2</sub> NPs). Hematological parameters, including hemoglobin (HGB), white blood cell count (WBC), and platelets, along with renal function tests such as blood urea nitrogen (BUN), creatinine, and urea, were assessed as conventional toxicity markers. Kidney tissue morphology was examined via histopathological analysis to detect structural alterations. Pharmacokinetic profiling revealed high bioavailability of CoI<sub>2</sub> NPs, though their ability to cross the blood–brain barrier was limited. Molecular docking identified the binding interactions of cobalt ions with renal proteins, suggesting potential disruptions in protein structure and function. Furthermore, results showed significant hematological and renal effects, with increased HGB levels in the high-dose group (14.23 ± 0.57&#xa0;g/dL) and elevated WBC (7.6 ± 1 × 10<sup>3</sup>/µL), indicating inflammation. Elevated BUN (112 ± 1.5&#xa0;mg/dL) and creatinine (1.3 ± 0.03&#xa0;mg/dL) levels further suggested renal dysfunction. Histopathological analysis revealed tubular necrosis, hypertrophy, inflammation, and fibrosis, primarily in high-dose samples. In addition, the antioxidant activity of the engineered nanoparticles was evaluated through modulation of reactive oxygen species and enhancement of endogenous antioxidant defense mechanisms, indicating their potential role in mitigating oxidative stress–associated diabetic complications. The study concludes that CoI<sub>2</sub> NPs cause notable hematotoxicity and renal toxicity within 30&#xa0;days of exposure, emphasizing the need for careful dose management in biomedical applications to mitigate potential health risks.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Cobalt nanostructures induced hematotoxicity and renal toxicity in albino mice: an experimental and computational evaluation

  • 期刊论文

  • 发表日期：

    2026年3月18日

查看全文
  • Ali Umar,
  • Muhammad Saleem Khan,
  • Muhammad Wajid

摘要

The present study aims to evaluate the hematotoxicity and renal toxicity of cobalt iodide nanoplates (CoI2 NPs) in albino mice, validated through pharmacokinetic and molecular docking analyses. CoI2 NPs were synthesized and characterized for morphology, crystalline structure, and functional groups using scanning electron microscopy (SEM), X-ray diffraction (XRD), and Fourier transform infrared spectroscopy (FTIR), respectively. Albino mice were divided into control and treatment groups (low dose 2.27 mg/kg, high dose 4.55 mg/kg CoI2 NPs). Hematological parameters, including hemoglobin (HGB), white blood cell count (WBC), and platelets, along with renal function tests such as blood urea nitrogen (BUN), creatinine, and urea, were assessed as conventional toxicity markers. Kidney tissue morphology was examined via histopathological analysis to detect structural alterations. Pharmacokinetic profiling revealed high bioavailability of CoI2 NPs, though their ability to cross the blood–brain barrier was limited. Molecular docking identified the binding interactions of cobalt ions with renal proteins, suggesting potential disruptions in protein structure and function. Furthermore, results showed significant hematological and renal effects, with increased HGB levels in the high-dose group (14.23 ± 0.57 g/dL) and elevated WBC (7.6 ± 1 × 103/µL), indicating inflammation. Elevated BUN (112 ± 1.5 mg/dL) and creatinine (1.3 ± 0.03 mg/dL) levels further suggested renal dysfunction. Histopathological analysis revealed tubular necrosis, hypertrophy, inflammation, and fibrosis, primarily in high-dose samples. In addition, the antioxidant activity of the engineered nanoparticles was evaluated through modulation of reactive oxygen species and enhancement of endogenous antioxidant defense mechanisms, indicating their potential role in mitigating oxidative stress–associated diabetic complications. The study concludes that CoI2 NPs cause notable hematotoxicity and renal toxicity within 30 days of exposure, emphasizing the need for careful dose management in biomedical applications to mitigate potential health risks.