- Academic Editor
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Background: The impact of melatonin on bisphenol A (BPA)-induced
testicular apoptosis and endoplasmic reticulum (ER) stress was explored.
Methods: The mice received BPA (50 mg/kg) by gavage for 30 days while
being injected with 20 mg/kg melatonin. Protein expressions were detected with
western blotting. The Terminal Deoxynucleotidyl Transferase dUTP Nick End
Labeling (TUNEL) assay measured testicular cell apoptosis. Testosterone was
quantified by employing enzyme-linked immunosorbent assay (ELISA).
Results: Melatonin promoted the development of seminiferous tubules,
restored the orderly arrangement of the germ cells, and increased epithelial
layers in the seminiferous tubules in BPA-treated mice. Moreover, in BPA-treated
mouse testicular cells, melatonin markedly upregulated melatonin receptor 1A
(MTNR1A) and melatonin Receptor 2 (MTNR2) expressions while downregulating ER
molecular chaperones glucose-regulated protein 78 (GRP78) and glucose-regulated
protein 94 (GRP94). Furthermore, it decreased p-PERK, p-IRE1, and ATF6