Nitric oxide (NO) plays a role in estrogen-mediated uterine receptivity. We hypothesize that L-arginine a NO substrate will increase NO production and boost pregnancy outcomes in rats with inhibited NO synthase activity. Thirty-two pregnant rats were randomly divided into four groups, control (10 mL/kg of water), L-NAME (50 mg/kg), L-NAME + L-Arg (50 mg/kg and 500 mg/kg) and L-Arg only (500 mg/kg). L-Arg and L-NAME were administered orally and subcutaneously respectively from day 3-11 of pregnancy. Blood samples were collected on day 8 for the assay of nitric oxide, TNF-α and interleukin-10 concentrations. The rats were sacrificed on day 12 of pregnancy. L-NAME-administered rats had decreased maternal body weight and number and weight of implantation sites when compared with the control (p< 0.05). Co-administration of L-NAME with L-Arg significantly increased the body weights and fetal weights when compared with L-NAME. L-Arginine co-administration with L-NAME significantly boosted NO and interleukin-10 concentrations and significantly reduced TNF-α concentration when compared with L-NAME. Malondialdehyde (MDA) level was significantly reduced while activities of superoxide dismutase (SOD) and catalase (CAT) increased in the L-NAME + L-Arg group compared with L-NAME only group. The study reveals that L-arginine improves fetal development through its antioxidant and anti-inflammatory actions.
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