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Post-pubertal Susceptibility to Cadmium-Induced Cardiac Injury: Role of Metallothionein, Antioxidant Defense, and

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Post-pubertal female rats show greater cadmium-induced heart damage due to impaired metallothionein induction and hormonal changes, highlighting critical vulnerability windows.

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Area of Science:

  • Environmental toxicology
  • Cardiovascular toxicology
  • Endocrinology

Background:

  • Cadmium (Cd) is a pervasive environmental contaminant known to cause cardiotoxicity via endocrine disruption and oxidative stress.
  • Age-related differences in susceptibility to environmental toxins are increasingly recognized but not fully understood.
  • Understanding these age-related vulnerabilities is crucial for public health and risk assessment.

Purpose of the Study:

  • To investigate age-related differences in cadmium-induced cardiotoxicity in female rats.
  • To elucidate the underlying mechanisms, including oxidative stress, antioxidant status, and endocrine disruption.
  • To identify critical windows of vulnerability for environmental cadmium exposure.

Main Methods:

  • Comparison of pre-pubertal (30-day-old) and post-pubertal (60-day-old) female albino rats exposed to CdCl₂ (5.12 mg/kg/day) for 15 days.
  • Assessment of cadmium accumulation, cardiac injury markers (CK-MB, troponin I), electrocardiographic (ECG) changes, and infarct volume.
  • Evaluation of antioxidant status (glutathione, vitamin C, SOD, CAT, GPx) and metallothionein (MT) induction.
  • Analysis of adrenal function, including corticosterone (CORT) and estradiol (E2) levels, reflecting hypothalamic-pituitary-adrenal (HPA) axis activity.

Main Results:

  • Post-pubertal rats exhibited more severe cardiac injury despite lower cadmium accumulation compared to pre-pubertal rats.
  • Impaired metallothionein (MT) induction, depleted glutathione and vitamin C, and reduced antioxidant enzymes (SOD, CAT, GPx) were observed in post-pubertal animals.
  • Altered adrenal function, characterized by increased corticosterone (CORT) and decreased estradiol (E2), indicated differential HPA axis responsiveness.
  • Biomarkers confirmed cardiac vulnerability in post-pubertal rats, including elevated CK-MB and troponin I, ECG abnormalities, and larger infarct volumes.

Conclusions:

  • Post-pubertal susceptibility to cadmium cardiotoxicity is linked to reduced MT inducibility and HPA axis-mediated endocrine dysregulation.
  • These factors exacerbate oxidative injury and ventricular remodeling, leading to increased cardiac damage.
  • Adolescence and early adulthood represent critical windows of heightened vulnerability for females exposed to cadmium.
  • Variations in MT expression and estradiol levels may predict individual susceptibility, suggesting potential targets for intervention and stricter cadmium regulation.