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Acute Exposure to Bisphenol S Decreases In Vitro Right Atrial Contractility in Rats.

Jayanti Pant1, Radhika Agarwal1, Srikant S1

  • 1Physiology, All India Institute of Medical Sciences, Rishikesh, Rishikesh, IND.

Cureus
|January 31, 2024
PubMed
Summary
This summary is machine-generated.

Bisphenol S (BPS) exposure in rats reduced atrial contraction rate and force. This cardiotoxicity was mediated by a nitric oxide-dependent pathway, highlighting potential risks of BPA alternatives.

Keywords:
atrial contractilitybpscgmp independentnotoxicity

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Area of Science:

  • Toxicology
  • Cardiovascular Physiology
  • Environmental Health

Background:

  • Bisphenols, including Bisphenol A (BPA), are common in plastics.
  • Concerns over BPA toxicity have led to the use of alternatives like Bisphenol S (BPS).
  • Emerging evidence suggests BPS may also pose health risks, including cardiac effects.

Purpose of the Study:

  • To investigate the in vitro effects of Bisphenol S (BPS) on the contractile function of rat right atria.
  • To explore the underlying mechanisms of BPS-induced cardiac effects.

Main Methods:

  • Isolated rat right atria were used for in vitro studies.
  • Cumulative concentrations of BPS were applied to assess effects on atrial contractions.
  • Experiments included the use of antagonists like atropine, L-NAME, and methylene blue.

Main Results:

  • BPS significantly decreased both the rate and force of spontaneous atrial contractions.
  • The observed effects were not due to the ethanol solvent used for BPS.
  • L-NAME, but not atropine or methylene blue, antagonized the negative inotropic and chronotropic effects of BPS.

Conclusions:

  • BPS induces cardiotoxicity in rat atria.
  • The mechanism involves a nitric oxide (NO)-dependent pathway.
  • This NO-dependent pathway appears to be independent of cyclic guanosine monophosphate (cGMP).