1. Lipid peroxidation in bile: the role of hydrophobic bile acids and the effect on biliary epithelial cell function 
Nair Sreejayan, Christoph von Ritter 
Pathophysiology 
Volume 5, Issue 4, Pages (January 1999)
DOI: /S (98)

2. Fig. 1
Single electron reduction reactions of molecular oxygen. One electron reduction of oxygen, yields superoxide anion. A two electron reduction (dismutation reaction) results in the formation of hydrogen peroxide (a non radical). A further electron reduction (Fenton reaction) yields the cytotoxic hydroxyl radical.
Pathophysiology 1999 5, DOI: ( /S (98) )

3. Fig. 2
Chain events of lipid peroxidation. Initiation of lipid peroxidation may be mediated by any species which can abstract a hydrogen atom from polyunsaturated fatty acid (L) to yield the lipid alkyl radical (L). Lipid alkyl radicals can rapidly add oxygen to form lipid peroxyl radicals (LOO) which eventually liberate the lipid hydroperoxide (LOOH) via hydrogen abstraction from a neighboring allylic bond (which again generates a lipid radical furthering the chain reaction). The LOOH subsequently breaks down into a variety of cytotoxic aldehydic products which include nonealdehyde and malondialdehyde.
Pathophysiology 1999 5, DOI: ( /S (98) )

4. Fig. 3
The role of nuclear factor kappa-B in oxidant stress induced gene expression. Inactivated, NF-κB resides in the cytoplasm as a complex with the inhibitory I-κB. Cellular activation by a variety of stimuli, such as oxidant stress, results in the proteolytic degradation of I-κB followed by release I-κB from the complex. Consecutively, NF-κB gets translocated to the nucleus and interacts with regulatory NF-κB elements leading to the up-regulation of a variety of genes.
Pathophysiology 1999 5, DOI: ( /S (98) )

5. Fig. 4
Effect of oxidative stress and antioxidants on mucin secretion by cultured biliary epithelial cells. Dog gallbladder epithelial cells were grown to confluence in a transwell insert. The confluent monolayers were labeled with [3H]N-acetyl-d-glucosamine. The monolayers were then treated with the following pro-/anti-oxidant agents by placing them on the lower compartment (basolateral side of the epithelial cells) and incubating overnight at 37°C. (i) Polymorphonuclear cells (106 cells/ml) activated with phorbol myristate acetate (1 μM); (ii) activated polymorphonuclear cells (106 cells/ml)+catalase (1000 U/ml)+superoxide dismutase (500 U/ml); (iii) hydrogen peroxide (5 mM); (iv) hydrogen peroxide (5 mM)+desferal (2 mM); (v) malondialdehyde (3 μM). Mucin secretion was estimated by assessment of [3H]N-acetyl-d-glucosamine release in the culture medium in the upper compartment (apical side of the epithelial cells). Each treatment was performed in quadruplicate. The average counts/minute per well for the control wells was 1.5×103.. Activated polymorphonuclear cells, hydrogen peroxide and malondialdehyde induced a significant increase (*P<0.01) in mucin secretion by the gallbladder epithelial cells. Catalase-SOD combination completely inhibited the effect of PMN on epithelial cell mucin secretion while desferal abolished the effect of hydrogen peroxide.
Pathophysiology 1999 5, DOI: ( /S (98) )

6. Fig. 5
Effect of hydrophobic bile acids and biliary lipid peroxidation on biliary epithelial cell function (see text for details).
Pathophysiology 1999 5, DOI: ( /S (98) )