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.