Induction of the Expressions of Antioxidant Enzymes by Luteinizing Hormone in the Bovine Corpus Luteum

Abstract

Luteoprotective mechanisms of luteinizing hormone (LH) involved in the maintenance of bovine corpus luteum (CL) function have not been completely clarified. Since antioxidant enzymes are well documented as antiapoptotic factors in the CL of many mammals, we hypothesized that the luteoprotective action of LH is mediated by stimulating the local production and action of antioxidant enzymes. To test the above hypothesis, in the present study, we examined the mechanisms involved in the luteoprotective actions of LH. Cultured bovine luteal cells obtained from the CL at the mid-luteal stage (days 8–12 of the estrous cycle) were treated with LH (10 ng/ml), onapristone (OP; a specific progesterone receptor antagonist, 100 μM) and diethyldithiocarbamate [DETC; an inhibitor of superoxide dismutase (SOD), 100 μM] for 24 h. LH in combination with or without OP significantly increased the mRNA and protein expressions of manganese SOD (Mn-SOD) and catalase (CATA) and SOD activity. While LH alone significantly increased the mRNA and protein expressions of SOD containing copper and zinc (Cu,Zn-SOD), OP in combination with or without LH significantly decreased the mRNA and protein expressions of Cu,Zn-SOD. In addition, Cu,Zn-SOD, Mn-SOD and CATA mRNA expressions were higher at the mid luteal phase than the other luteal phases. LH in combination with DETC significantly decreased LH-increased cell viability. The overall results suggest that LH increases cell viability by LH-increased antioxidant enzymes, resulting in maintenance of CL function during the luteal phase in cattle.

Equilibrium between anti‐oxidants and reactive oxygen species: a requisite for oocyte development and maturation

“…This suggests the important role that ROS plays during the process of LH‐induced progesterone release. However, a study reported that LH also stimulates the intraluteal expressions of Copper/Zinc‐dependent SOD (Cu/Zn‐SOD), manganese‐dependent SOD (Mn‐SOD), and catalase to maintain the luteal cell viability and ROS balance . This study indicates that LH not only induces ROS production but also regulates it by stimulating the anti‐oxidant enzymes’ expression, thus maintaining the redox state.…”

“…In follicles, apart from mitochondrial respiration and oxidative phosphorylation, some other mechanisms also contribute to ROS release. Luteinizing hormone (LH) signals the corpus luteum to produce and secrete progesterone . The process is highly complex and regulated at several stages enlisted below.…”

“…Luteinizing hormone (LH) signals the corpus luteum to produce and secrete progesterone. 28 The process is highly complex and regulated at several stages enlisted below. Initially, after LH signaling, cholesterol is converted to pregnenolone in the mitochondria by cytochrome P450 side-chain cleavage that releases ROS.…”

Melatonin deprival modifies follicular and corpus luteal growth dynamics in a sheep model

“…LH regulates a variety of ovarian functions, although its main effect may be to stimulate P 4 secretion by the corpus luteum. In fact, LH strongly stimulates P 4 production by cultured bovine luteal cells (Juengel & Niswender 1999) and plays some luteoprotective roles by increasing luteal cell viability (Kawaguchi et al 2013).…”

Influence of manganese on apoptosis and glutathione content of cumulus cells during in vitro maturation in bovine oocytes

“…Manganese deficiency in cattle produces a delay in the first estrous (Bentley and Phillips, 1951;Rojas et al, 1965), and in small ruminants not only impairs estrous cycle, but also reduces birth weight (Underwood and Suttle, 1999). LH enhances the viability of lutheal cells by stimulating the intralutheal expression of Mn-SOD, Cu-Zn-SOD and catalase, and by stimulating SOD activity to maintain lutheal function in cows (Kawaguchi et al, 2013).…”