Oxidative Damage to Human Lens Epithelial Cells in Culture: Estrogen Protection of Mitochondrial Potential, ATP, and Cell Viability

Abstract

The present study indicates that both 17alpha- and 17beta-E(2) can preserve mitochondrial function, cell viability, and ATP levels in human lens cells during oxidative stress. Although the precise mechanism responsible for protection by the estradiols against oxidative stress remains to be determined, the ability of nonfeminizing estrogens, which do not bind to estrogen receptors, to protect against H(2)O(2) toxicity indicates that this conservation is not likely to be mediated through classic estrogen receptors.

Estrogen actions on mitochondria—Physiological and pathological implications

“…Pre-treatment with E2 ameliorated the H 2 O 2 -induced decline in cellular ATP (Wang et al, 2003b(Wang et al, , 2006. This ability of E2 to prevent pro-oxidant-induced declines in cellular ATP appears to be a general property of E2, as we have demonstrated a similar effect of E2 against H 2 O 2 -induced decline in cellular ATP in a non-neuronal, human lens cell type (Wang et al, 2003a). Furthermore, non-feminizing estrogens share this ability to protect ATP production (Wang et al, 2006).…”

“…We assessed the effects of estrogens on the production of ATP under two condition of stress to the mitochondria (Wang et al, 2001(Wang et al, , 2003a(Wang et al, , 2006. We first determined the effects on ATP production of 3-nitropropionic acid (3NPA), a succinate dehydrogenase inhibitor that uncouples oxidative phosphorylation, and the capacity of estrogens to ameliorate the effect on ATP of this mitochondrial toxin.…”

Rapid action of oestradiol against hydrogen peroxide-induced oxidative stress in cataractous lens epithelium: an in vitro study

“…1,18 The protective role of oestrogen in cataractogenesis has been well studied in in vivo and in vitro conditions. 5,6,12,15 This study elucidates the quick protective role of 17b-oestradiol against H 2 O 2 -induced oxidative stress in cultured LECs.…”

“…Oestradiol has been previously reported to preserve the mitochondrial function, cell viability, and intracellular ATP levels in cultured human LECs during oxidative stress. 12,26 Emerging published data suggest that these lipophilic hormones are also able to produce rapid effects within several seconds, which cannot be adequately explained through the classical mechanism. These rapid responses have been observed in several tissues, such as myometrial cells, neurons, endothelium, osteoblasts, granulosa cells, and some breast cancer cell lines.…”

“…8 The precise mechanism of these cytoprotective effects of oestrogen against H 2 O 2 in lens epithelial cells (LECs) is not known, but a plethora of cellular responses to the steroid has been reported, including the protection of the mitochondrial function, stimulation of antiapoptotic proteins, and stimulation of protective signalling pathways. [9][10][11] Wang et al 12 have demonstrated that oestrogens are potent cytoprotectants that preserve the mitochondrial function during H 2 O 2 -induced oxidant insult. Nevertheless, the exact mechanism of oestrogen action against oxidative stress is not known.…”