What intestinal volvulus?

Intestinal volvulus is a medical condition characterized by the twisting or rotation of a portion of the intestines around its mesentery, which is the supportive tissue that attaches the intestines to the abdominal wall. This twisting obstructs the normal flow of blood and contents through the intestine, leading to bowel obstruction, ischemia (lack of blood supply), and potentially necrosis (tissue death) if left untreated. Intestinal volvulus can occur anywhere along the gastrointestinal tract but most commonly affects the sigmoid colon (sigmoid volvulus) or the small intestine (small bowel volvulus).


What is the relationship between intestinal volvulus and oxidative stress?

The relationship between intestinal volvulus and oxidative stress is not well-studied, and there is limited direct evidence linking the two conditions. However, it is plausible that intestinal volvulus, particularly when complicated by bowel ischemia, could lead to oxidative stress through several mechanisms:


  • Ischemia-Reperfusion Injury: Intestinal volvulus causes twisting of the intestines, which can lead to impaired blood flow (ischemia) to the affected portion of the bowel. When the volvulus is relieved, either spontaneously or through surgical intervention, blood flow may be restored (reperfusion). This process of ischemia followed by reperfusion can lead to ischemia-reperfusion injury, characterized by the generation of reactive oxygen species (ROS) during reperfusion. ROS production during reperfusion can overwhelm antioxidant defenses, leading to oxidative stress and tissue damage in the affected intestine.


  • Inflammatory Response: Bowel ischemia resulting from intestinal volvulus triggers an inflammatory response, characterized by the release of pro-inflammatory cytokines, activation of immune cells, and recruitment of inflammatory mediators to the site of injury. Inflammatory processes generate ROS as byproducts of immune cell activation and respiratory burst reactions. Excessive ROS production during inflammation overwhelms antioxidant defenses and leads to oxidative stress, exacerbating tissue injury and inflammation in the affected intestine.


  • Mitochondrial Dysfunction: Ischemia-reperfusion injury in the intestine can impair mitochondrial function, leading to increased production of ROS within the affected cells. Mitochondria are the primary site of ROS production in cells, and mitochondrial dysfunction can lead to oxidative stress and cellular damage. Ischemia-induced mitochondrial dysfunction may contribute to oxidative stress and exacerbate tissue injury in the setting of intestinal volvulus.


  • Activation of Redox Signaling Pathways: Ischemia-reperfusion injury and inflammatory processes associated with intestinal volvulus can activate redox-sensitive signaling pathways, such as nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. These signaling pathways regulate gene expression, inflammatory responses, and cell survival pathways in response to oxidative stress. Dysregulation of redox signaling pathways can further exacerbate oxidative stress and contribute to tissue damage in the affected intestine.


While these mechanisms suggest a potential role for oxidative stress in the pathophysiology of intestinal volvulus, further research is needed to elucidate the specific contributions of oxidative stress to the development and progression of this condition.