Table 1.

Summaries of the disruptive effects of BPA in the animal in vitro studies ¹.

Drugs	Concentration	Animals/Organs/Cells	Results	References
BPA and Penitrem	10 µmol/L 1 µmol/L	Canine coronary smooth muscle cells AD 293 cells	▪Activated an external current in smooth muscle cells previously inhibited by penitrem ▪Increased Maxi-K activity	[35]
BPA and/or 17β-estradiol(E2)-	1 nmol/L	Ventricular myocytes and Sprague Dawley adult mice heart and ERβ knockout mice (Erβ−/−)	▪Rapid induced arrhythmogenic effect in females ▪Pronounced when combined with estradiol ▪Ventricular arrhythmias ▪Rapidly altered myocyte Ca2+ handling ▪Increased sarcoplasmic reticulum leak ▪Ryanodine inhibition of SR Ca2+ leak suppressed estrogen-induced triggered activities.	[45]
BPA and/or E2	0.001–1 nmol/L	Rat Sprague Dawley myocytes and female knockout Erβ mice.	▪Concentration–response curve for stimulatory effects (contractility and arrhythmogenic) of BPA and E2 in female myocytes was inverted-U-shaped ▪Rapid arrhythmogenic effects	[46]
BPA	1–100 µmol/L	HEK293 cells transfected with Human Cardiac Sodium Channel	▪BPA induced a dose-dependent tonic block of the human Nav1.5 sodium channel	[43]
BPA or BPA and E2	1 nmol/L	Adult Sprague Dawley rats’ hearts	▪Increase in the duration of sustained ventricular arrhythmias ▪Increased ventricular fibrillation duration ▪Pro-arrhythmic effects of estrogens abolished by MPP combined with PHTPP ▪Reduced infarction size	[47]
BPA	1 nmol/L	Female rat ventricular myocytes	▪BPA rapidly activated two parallel signaling pathways, the cAMP/PKA pathway, and the PLC/IP3/Ca2+/CAMKII pathway.	[48]
BPA	1–100 μmol/L	Mouse cardiac myocytes	▪BPA interacted with calcium channels by binding to an external site outside the pore-forming region	[38]
BPA membrane-impermeant BPA-monosulfate (BPA-MS)	100 µmol/L	AD 293 cells expressing α or α + β1 subunits	▪Increased BK channel activity	[36]
BPA	1–100 μmol/L	HEK 293 cells transfected with CaV3.1-CaV3.3	▪BPA inhibited T-type calcium channels ▪Low (nanomolar) concentrations inhibited only a minor part of channels ▪Micromolar concentrations blocked the channel in both open and inactivated states.	[39]
BPA	0.1 nmol/L−1–1 μmol/L	Female rat ventricular myocytes	▪Inverted-U-shaped dose–response	[40]
BPA	0.001–100 µmol/L	Neonatal rat cardiomyocytes	▪Reduced Ca2+ transient amplitude ▪Prolonged Ca2+ transient release time	[54]
BPA	0.001–100 µmol/L	A7R5 cells from rat aorta	▪Inhibition of L-type calcium channels	[37]
BPA	100 µmol/L	Neonatal rat cardiomyocytes	▪Reduced the spontaneous beating rate and increased beat rate variability. ▪Diminished calcium transient amplitudes, prolonged calcium transient upstroke and duration time.	[50]
BPA	1–100 µmol/L	Zebrafish larvae Zebrafish cell lines	▪BPA, BPAF, and BPC were agonists with different potencies for the three zebrafish estrogen receptors	[49]
BPA and/or PFOS	25 μmol/L for 14 days	Rat cardiomyocytes	▪Increased level of total collagen and dynamin-associated protein 1 mRNA ▪Decrease in mitochondrial length and ATP level	[52]
BPA	0–10 µmol/L BPA for 24 h	Murine aortic ECs (MAECs) and H9c2 cells.	▪Increased the expression of RIP 3 ▪Increased expression of inflammatory cytokines	[53]
BPA	1–100 μmol/L	hiPSC-CM	▪BPA exposure inhibited Ca2+ transients and cardiac contraction ▪BPA exposure affected Cav1.2, Nav1.5, and hERG channel activity.	[41]
BPA Bisphenol S Bisphenol F	0.0–100 µmol/L	hiPSC-CM	▪BPA was the most potent inhibitor of the sodium channel, L-type Ca2+ channel, and hERG channel current	[42]

¹ Legend: BPA—bisphenol A; Ca²⁺—calcium; hiPSC-CMs—human-induced pluripotent stem-cell-derived cardiomyocytes; PFOS—perfluorooctane sulfonate.