What is obstructive jaundice?

Obstructive jaundice, also known as cholestatic jaundice, is a medical condition characterized by the accumulation of bilirubin in the blood due to obstruction of the bile ducts. Bilirubin is a yellow pigment produced during the breakdown of red blood cells and is normally processed by the liver and excreted in bile. When the flow of bile from the liver to the intestine is blocked, bilirubin cannot be properly eliminated from the body, leading to its buildup in the bloodstream and subsequent yellowing of the skin and eyes (jaundice).


Obstructive jaundice can result from various conditions that obstruct the bile ducts, including:


  • Gallstones: Small, hard deposits of cholesterol or bilirubin that can form in the gallbladder or bile ducts and block the flow of bile.


  • Bile Duct Stones: Stones that form within the bile ducts themselves, obstructing the flow of bile.


  • Biliary Strictures: Narrowing or scarring of the bile ducts due to inflammation, infection, trauma, or other causes.


  • Biliary Tumors: Benign or malignant tumors that develop within or near the bile ducts and obstruct the flow of bile.


  • Pancreatic Tumors: Tumors of the pancreas can compress or invade the bile ducts, leading to obstruction.


  • Pancreatitis: Inflammation of the pancreas can cause swelling and compression of the bile ducts, resulting in obstruction.


  • Parasitic Infections: Parasitic infections such as liver flukes can obstruct the bile ducts and cause jaundice.


What is the relationship between obstructive jaundice and oxidative stress?

The relationship between obstructive jaundice and oxidative stress is multifaceted and involves several interconnected mechanisms:


  • Bilirubin Metabolism: Obstructive jaundice leads to impaired excretion of bilirubin, a yellow pigment produced during the breakdown of red blood cells. Bilirubin is a potent antioxidant that helps neutralize reactive oxygen species (ROS) and protect cells from oxidative damage. However, in obstructive jaundice, the buildup of bilirubin in the bloodstream may overwhelm the antioxidant capacity of the body, leading to oxidative stress.


  • Bile Duct Obstruction: The obstruction of bile ducts in obstructive jaundice results in the accumulation of bile in the liver and bloodstream. Bile contains bile acids, which are amphipathic molecules with detergent properties. Under normal conditions, bile acids help solubilize and excrete bilirubin and other waste products from the liver. However, in obstructive jaundice, the retention of bile acids can lead to bile acid-induced oxidative stress. Bile acids can promote the formation of ROS and induce oxidative damage to hepatocytes (liver cells) and other tissues.


  • Inflammatory Response: Bile duct obstruction triggers an inflammatory response characterized by the activation of immune cells, release of pro-inflammatory cytokines, and recruitment of inflammatory mediators to the site of injury. Chronic inflammation contributes to oxidative stress by stimulating the production of ROS and reactive nitrogen species (RNS) by immune cells such as macrophages and neutrophils. In turn, oxidative stress amplifies the inflammatory response, forming a vicious cycle that exacerbates tissue damage and dysfunction.


  • Ischemia-Reperfusion Injury: In cases of severe bile duct obstruction or surgical interventions to relieve the obstruction, ischemia-reperfusion injury can occur. Ischemia refers to the deprivation of oxygen and nutrients to tissues due to reduced blood flow, while reperfusion refers to the restoration of blood flow following ischemia. Ischemia-reperfusion injury can lead to oxidative stress and tissue damage due to the generation of ROS during reperfusion. The liver is particularly vulnerable to ischemia-reperfusion injury, which can further exacerbate liver dysfunction in obstructive jaundice.


Overall, obstructive jaundice induces oxidative stress through various mechanisms, including impaired bilirubin metabolism, bile acid-induced toxicity, inflammation, and ischemia-reperfusion injury.