Effects of lead (Pb) exposure during gestation and lactation on female pubertal development in the rat

Robert K Dearth1, Jill K Hiney, Vinod Srivastava

  • 1Department of Veterinary Anatomy & Public Health, Texas A&M University, College Station, TX 77843-4458, USA.

Insights

Lead exposure during pregnancy or lactation delays female puberty by suppressing key hormones like IGF-1, LH, and estradiol. These detrimental effects occur even at low blood lead levels, highlighting critical developmental risks.

Area of Science:

  • Environmental Toxicology
  • Reproductive Endocrinology
  • Developmental Biology

Background:

  • Lead (Pb) exposure is known to delay sexual maturation, but the precise mechanisms and critical exposure windows remain unclear.
  • Understanding the impact of low-level lead exposure on reproductive development is crucial for public health.
  • Previous research indicates potential disruptions in puberty-related hormones, but detailed insights are lacking.

Purpose of the Study:

  • To investigate the effects of gestational and/or lactational lead exposure on the onset of female puberty.
  • To determine the relationship between maternal and fetal lead levels and subsequent pubertal hormone changes.
  • To elucidate the role of insulin-like growth factor-1 (IGF-1) in lead-induced pubertal delay.

Main Methods:

  • Adult female rats were exposed to lead acetate (PbAc) or sodium acetate (control) during gestation and/or lactation.
  • Cross-fostering was used to isolate exposure during gestation only, lactation only, or both.
  • Blood and tissue lead levels, puberty onset, and serum levels of IGF-1, luteinizing hormone (LH), and estradiol (E2) were measured.

Main Results:

  • Lead exposure significantly delayed the onset of puberty in female rats.
  • Delayed puberty was associated with suppressed serum levels of IGF-1, LH, and E2.
  • Lead exposure did not affect liver IGF-1 mRNA levels, suggesting post-transcriptional regulation of IGF-1.
  • Detrimental effects were observed regardless of exposure timing, with gestational exposure showing higher sensitivity.
  • Observed effects occurred at blood lead levels lower than previously reported, relevant to human health.

Conclusions:

  • Lead exposure disrupts the normal timing of female puberty, likely by interfering with IGF-1 synthesis or secretion.
  • The findings suggest that lead's detrimental effects on puberty onset are mediated by suppressed circulating IGF-1, impacting LH release.
  • Gestational lead exposure appears particularly sensitive, and effects are seen at environmentally relevant low lead levels.

Related Concept Videos