White adipose tissue (WAT) plays an important role in
obesity pathophysiology. Redox signaling underlies several aspects of WAT physiology; however, the
thiol redox environment of WAT has not yet been fully characterized. Dietary and
endocrine disrupting chemical (EDC) exposures during development can transiently impact the cellular redox environment, but it is unknown whether these exposures can reprogram the WAT
thiol redox environment. To characterize the WAT
thiol redox environment, we took a descriptive approach and measured
thiol redox parameters using high-performance liquid chromatography in mouse mesenteric (mWAT), gonadal (gWAT) and subinguinal (sWAT) depots.
Cysteine (CYSS:CYS) and
glutathione (
GSSG:GSH) redox potentials (Eh) were more oxidizing in gWAT and sWAT than mWAT. Increased
body weight, relative WAT weight and age were associated with oxidizing
GSSG:GSH Eh in mWAT in a sex-specific manner.
Body weight and relative WAT weight were also positively associated with
GSSG:GSH Eh in sWAT. We carried out a second mouse study with perinatal exposures to
bisphenol A (BPA) and Mediterranean and Western high-fat diets (HFDs) to determine whether early-life chemical and dietary factors have long-lasting impacts on mWAT redox parameters. Mice exposed to Mediterranean HFD or BPA had more oxidizing
GSSG:GSH mWAT Eh than controls, with more pronounced differences in females. These findings suggest an important role for the
thiol redox environment in WAT physiology. Observed sex-specific and depot-specific differences in
thiol redox parameters are consistent with known WAT physiology. Lastly, mWAT
GSSG:GSH Eh may be reprogrammed by developmental exposure to HFDs and EDCs, which may have implications for
obesity risk.