Malondialdehyde, nitric oxide and adrenomedullin levels in patients with primary dysmenorrhea

Abstract

In conclusion, the results of this study showed that the serum levels of MDA, NO, and AM increase in subjects with primary dysmenorrhea, suggesting the possibility that lipid peroxidation and oxidative stress play a significant role in the etiopathogenesis of primary dysmenorrhea.

Ligustilide prevents LPS-induced iNOS expression in RAW 264.7 macrophages by preventing ROS production and down-regulating the MAPK, NF-κB and AP-1 signaling pathways

“…AS has been used to regulate menstruation, an inflammatory syndrome, in Asia for thousands of years. Inflammatory mediators, such as PGE 2 [3], NO [4] and TNF-α [5], are elevated in the serum and peritoneal fluid of primary dysmenorrheal subjects. NF-κB is thought to promote and maintain endometriosis [6].…”

Investigation of oxidative balance in patients with dysmenorrhea by multiple serum markers

“…Dysmenorrhea also has been reported to lead to an increase in lipid peroxidation, an index of oxidative stress (8). Previous studies about OS and dysmenorrhea investigated only malondialdehyde (MDA) levels as a marker of oxidative status (9,10). However, measuring MDA levels is limited in detecting oxidative stress in some cases, and might not be sufficient to show real oxidative stress in dysmenorrhoea (11,12).…”

Non-steroidal anti-inflammatory drug modulates oxidative stress and calcium ion levels in the neutrophils of patients with primary dysmenorrhea

“…When a bacterial infection occurs, increased [Ca 2+ ] i due to release from intracellular stores and entry into neutrophils via VGCC and TRP channels is a key initiator of activation, leading to increased ROS production and providing a means of attacking the bacteria (Dikensoy et al, 2008;Bréchard and Tschirhart, 2008). In chronic inflammatory disease, however, this mechanism contributes to the development of oxidative damage.…”

“…Increased levels of proinflammatory cytokines, interleukins (Yeh et al, 2004), and tumor necrosis factor-␣ (TNF-␣), neutrophil hyperfunction (Marchini et al, 1995), and excessive reactive oxygen species (ROS) production (Marchini et al, 1995;Dikensoy et al, 2008) have been reported in patients with primary dysmenorrhea. Neutrophils are cells that play an important role in immune responses (Ayub and Hallett, 2004).…”

“…This can trigger the accumulation of free radicals, such as ROS (Sirmali et al, 2007). Free radicals are the products of biological reduction reactions (Nazıroglu, 2007), and overproduction of ROS has been implicated in the pathogenesis of dysmenorrhea (Dikensoy et al, 2008). ROS can cause disease and cell damage by damaging other molecules, including proteins, lipids, and DNA.…”