Bisphenol A regulation of testicular endocrine function in male rats is affected by diet.
There is concern that early-life exposure to bisphenol A (BPA) may alter developmental programming and predispose individuals to obesity and reproductive anomalies. The present study was designed to determine if a high fat diet at sexual maturation moderates testicular toxicity occasioned by exposure to BPA during reproductive development. Therefore, male rats were exposed to BPA by maternal gavage (0, 2.5 or 25 μg/kg body weight/day) from gestational day 12 to postnatal day 21. At weaning, control and BPA-exposed animals were placed on a regular normal fat diet (NFD) until 70 days of age when they were continued on the NFD or were maintained on a high fat diet (HFD) until euthanasia at 98 days. Adult male rats maintained on HFD were generally heavier than NFD animals due to greater energy intake but energy intake per unit body weight gain was similar in all animals. However, perinatal exposure to BPA decreased (P<0.05) serum adiponectin as well as adiponectin and AdipoR2 protein expression levels in Leydig cells. Importantly, the combination of BPA exposure and HFD consumption promoted lipid peroxidation evidenced by elevated serum thiobarbituric acid reactive substances and glutathione concentrations. These findings imply that interaction between BPA and HFD potentially causes testicular dysfunction to a greater degree than would be due to BPA exposure or HFD consumption. Given the relationship that exists between energy homeostasis and reproductive activity, additional studies are warranted to investigate the consequences of BPA-diet interactions on testicular function.
Department of Anatomy, Physiology and Pharmacology, Auburn AL 36849, United States.
Manjunatha K
MK
Nanjappa
Department of Pharmacal Sciences, Auburn University, Auburn AL 36849, United States.
Manuj
M
Ahuja
Department of Pharmacal Sciences, Auburn University, Auburn AL 36849, United States.
Muralikrishnan
M
Dhanasekaran
Department of Anatomy, Physiology and Pharmacology, Auburn AL 36849, United States.
Elaine S
ES
Coleman
Department of Anatomy, Physiology and Pharmacology, Auburn AL 36849, United States.
Tim D
TD
Braden
Department of Anatomy, Physiology and Pharmacology, Auburn AL 36849, United States.
Frank F
FF
Bartol
Department of Pathobiology, Auburn University, Auburn AL 36849, United States.
R Curtis
RC
Bird
Department of Anatomy, Physiology and Pharmacology, Auburn AL 36849, United States.
Desiree
D
Wanders
Department of Anatomy, Physiology and Pharmacology, Auburn AL 36849, United States.
Robert L
RL
Judd
Department of Anatomy, Physiology and Pharmacology, Auburn AL 36849, United States. Electronic address: akingbt@auburn.edu.
Benson T
BT
Akingbemi
D052242:Adiponectin / Q000097:blood; D000818:Animals; D001559:Benzhydryl Compounds / Q000633:toxicity*; D015153:Blotting, Western; D001835:Body Weight / Q000502:physiology; D059305:Diet, High-Fat / Q000009:adverse effects*; D004958:Estradiol / Q000097:blood; D004968:Estrogens, Non-Steroidal / Q000633:toxicity*; D005260:Female; D007985:Leydig Cells / Q000187:drug effects / Q000378:metabolism; D008297:Male; D010636:Phenols / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D020318:Rats, Long-Evans; D054419:Receptors, Adiponectin / Q000097:blood; D012741:Sexual Maturation / Q000187:drug effects* / Q000502:physiology; D013737:Testis / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D013739:Testosterone / Q000097:blood; D000098826:Bisphenol A Compounds
D052242:Adiponectin; D001559:Benzhydryl Compounds; D004958:Estradiol; D004968:Estrogens, Non-Steroidal; D010636:Phenols; D054419:Receptors, Adiponectin; D013739:Testosterone; C506573:adiponectin receptor 2, rat; C006780:bisphenol A; D000098826:Bisphenol A Compounds
Adiponectin; Leydig cells; Oxidative stress; Steroid hormones; Xenoestrogen