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Evidence that glutathione depletion is a mechanism responsible for the anti-inflammatory effects of ethyl pyruvate in cultured lipopolysaccharide-stimulated RAW 264.7 cells

This pathomechanism is mainly associated with Ca2+-facilitated mitochondrial permeability transition, followed by release of mitochondrial pro-apoptotic factors and impairment of the electron transport chain, leading eventually to ATP depletion and necrotic cell death.9596 ii) Impairment of the bile salt-dependent fraction of the bile flow due to competitive inhibition of bile salt transport by the intracellular GSSG formed in excess during the oxidative challenge.70,72 This is supported by the fact that GSSG cis-inhibits the transport of the model bile salt, taurocholate, in liver canalicular membrane vesicles.97 In line with this contention, mirror curves depicting an increase in biliary excretion of GSSG and a decrease in biliary excretion of bile salts were obtained by administrating different pro-oxidant compounds in the isolated rat perfused liver, such as hydrogen peroxide,72 menadione92 and tBOOH.70,72 Furthermore, an inverse relationship between intracellular GSSG content and the percentage of inhibition of the biliary bile salt output was obtained by manipulating GSSG content using different oxidizing compounds, in the presence or absence of inhibitors of GSSG formation.72,92 iii) Impairment of the bile salt-independent bile flow due to a decrease in the biliary excretion of total glutathione (GSH plus GSSG)

As non-heme iron-containing dioxygenases, lipoxygenases (LOXs) directly catalyze the peroxidation of PUFAs, both free and esterified in phospholipids (77, 78)