Biochemical markers in a porcine model of adult respiratory distress syndrome induced by endotoxemia

LRP1 Shedding in Ricin-Induced Lung Injury: A Cell-Specific Response to Toxin Exposure

“…Additionally, the release of soluble LRP1 (sLRP1) into the extracellular space appears to have far-reaching consequences beyond the immediate effects on LRP1-mediated signaling by inhibiting the endocytosis of other crucial ligands of the membrane-bound LRP1 receptor such as urokinase (uPA), tissue-type plasminogen activators (tPA), thrombospondin and fibronectin. These molecules play pivotal roles in various aspects of the inflammatory response, including extracellular matrix remodeling, cell adhesion, and proteolytic cascades [ 66 , 67 , 68 ]. By interfering with their endocytosis, LRP1 shedding may lead to their accumulation in the extracellular space, potentially exacerbating inflammatory conditions.…”

LRP1 Shedding in Ricin-Induced Lung Injury: A Cell-Specific Response to Toxin Exposure

“…Additionally, the release of soluble LRP1 (sLRP1) into the extracellular space appears to have far-reaching consequences beyond the immediate effects on LRP1-mediated signaling by inhibiting the endocytosis of other crucial ligands of the membrane-bound LRP1 receptor such as urokinase (uPA), tissue-type plasminogen activators (tPA), thrombospondin and fibronectin. These molecules play pivotal roles in various aspects of the inflammatory response, including extracellular matrix remodeling, cell adhesion, and proteolytic cascades [ 66 , 67 , 68 ]. By interfering with their endocytosis, LRP1 shedding may lead to their accumulation in the extracellular space, potentially exacerbating inflammatory conditions.…”

Use of Acetylcysteine as the Life-saving Antidote in Amanita phalloides (Death Cap) Poisoning

“…to counteract the oxidative damage provoked by α-amanitin, often with liver transplantation as the only life saving solution [3], in the Department of Intensive Care of the University Hospital of Messina (Italy), has been developed a protocol for the treatment of amanita mycestism based on N-acetyl-cysteine 1) (CAS 616-91-1, NAC), according to the paracetamol poisoning treatment protocol, given the same hepatocellular damage brought about by both α-amanitin and paracetamol. NAC is an oxygen free radicals savenger, easily penetrating into cells by virtue of its liposolubility, supplying intracellular depleted gluthatione (GSH) pool [13,18], further blocking the acute toxicity of tumor necrosis factor α (TNF-α), at a gene transcription level (inhibition of MAPK-JNK (Mitogen Activating Protein Kinase Type Ink)) [14], increasing the splancnic DO 2 (splancnic oxygen delivery) (sDO 2 ) and modulating platelet aggregability by acting on the nitric oxide (NO) production [15,16]. Some investigators [17] report, in patients with FHF, an increase of DO 2 , VO 2 and O 2 ER (oxygen extraction ratio) occurred after infusion of NAC.…”

Alterations in the functions of the reticuloendothelial and protease-antiprotease systems after intraperitoneal injection of zymosan in rats

“…It is a well known antioxidant with multiple functions (24), and is mainly metabolised to cysteine (a precursor in the biosynthesis of glutathione); it increases glutathione and sulfhydryl concentrations, and reduces hydrogen peroxide-dependent injury by inactivating the hypochlorous acid and hydroxyl radicals formed by hydrogen peroxide (2). NAC may also have beneficial effects, such as decreasing neutrophil-aggregating activity and increasing cardiac output and oxygen delivery (25). The reducing effect of NAC on production of tumour necrosis factor (TNF) is most likely caused by a decreased release of oxygen free radicals (29).…”

LRP1 Shedding in Ricin-Induced Lung Injury: A Cell-Specific Response to Toxin Exposure

“…Additionally, the release of soluble LRP1 (sLRP1) into the extracellular space appears to have far-reaching consequences beyond the immediate effects on LRP1-mediated signaling by inhibiting the endocytosis of other crucial ligands of the membrane-bound LRP1 receptor such as urokinase (uPA), tissue-type plasminogen activators (tPA), thrombospondin and fibronectin. These molecules play pivotal roles in various aspects of the inflammatory response, including extracellular matrix remodeling, cell adhesion, and proteolytic cascades [ 66 , 67 , 68 ]. By interfering with their endocytosis, LRP1 shedding may lead to their accumulation in the extracellular space, potentially exacerbating inflammatory conditions.…”

Use of Acetylcysteine as the Life-saving Antidote in Amanita phalloides (Death Cap) Poisoning

“…to counteract the oxidative damage provoked by α-amanitin, often with liver transplantation as the only life saving solution [3], in the Department of Intensive Care of the University Hospital of Messina (Italy), has been developed a protocol for the treatment of amanita mycestism based on N-acetyl-cysteine 1) (CAS 616-91-1, NAC), according to the paracetamol poisoning treatment protocol, given the same hepatocellular damage brought about by both α-amanitin and paracetamol. NAC is an oxygen free radicals savenger, easily penetrating into cells by virtue of its liposolubility, supplying intracellular depleted gluthatione (GSH) pool [13,18], further blocking the acute toxicity of tumor necrosis factor α (TNF-α), at a gene transcription level (inhibition of MAPK-JNK (Mitogen Activating Protein Kinase Type Ink)) [14], increasing the splancnic DO 2 (splancnic oxygen delivery) (sDO 2 ) and modulating platelet aggregability by acting on the nitric oxide (NO) production [15,16]. Some investigators [17] report, in patients with FHF, an increase of DO 2 , VO 2 and O 2 ER (oxygen extraction ratio) occurred after infusion of NAC.…”

Alterations in the functions of the reticuloendothelial and protease-antiprotease systems after intraperitoneal injection of zymosan in rats

“…It is a well known antioxidant with multiple functions (24), and is mainly metabolised to cysteine (a precursor in the biosynthesis of glutathione); it increases glutathione and sulfhydryl concentrations, and reduces hydrogen peroxide-dependent injury by inactivating the hypochlorous acid and hydroxyl radicals formed by hydrogen peroxide (2). NAC may also have beneficial effects, such as decreasing neutrophil-aggregating activity and increasing cardiac output and oxygen delivery (25). The reducing effect of NAC on production of tumour necrosis factor (TNF) is most likely caused by a decreased release of oxygen free radicals (29).…”

LRP1 Shedding in Ricin-Induced Lung Injury: A Cell-Specific Response to Toxin Exposure

“…Additionally, the release of soluble LRP1 (sLRP1) into the extracellular space appears to have far-reaching consequences beyond the immediate effects on LRP1-mediated signaling by inhibiting the endocytosis of other crucial ligands of the membrane-bound LRP1 receptor such as urokinase (uPA), tissue-type plasminogen activators (tPA), thrombospondin and fibronectin. These molecules play pivotal roles in various aspects of the inflammatory response, including extracellular matrix remodeling, cell adhesion, and proteolytic cascades [ 66 , 67 , 68 ]. By interfering with their endocytosis, LRP1 shedding may lead to their accumulation in the extracellular space, potentially exacerbating inflammatory conditions.…”

Use of Acetylcysteine as the Life-saving Antidote in Amanita phalloides (Death Cap) Poisoning

“…to counteract the oxidative damage provoked by α-amanitin, often with liver transplantation as the only life saving solution [3], in the Department of Intensive Care of the University Hospital of Messina (Italy), has been developed a protocol for the treatment of amanita mycestism based on N-acetyl-cysteine 1) (CAS 616-91-1, NAC), according to the paracetamol poisoning treatment protocol, given the same hepatocellular damage brought about by both α-amanitin and paracetamol. NAC is an oxygen free radicals savenger, easily penetrating into cells by virtue of its liposolubility, supplying intracellular depleted gluthatione (GSH) pool [13,18], further blocking the acute toxicity of tumor necrosis factor α (TNF-α), at a gene transcription level (inhibition of MAPK-JNK (Mitogen Activating Protein Kinase Type Ink)) [14], increasing the splancnic DO 2 (splancnic oxygen delivery) (sDO 2 ) and modulating platelet aggregability by acting on the nitric oxide (NO) production [15,16]. Some investigators [17] report, in patients with FHF, an increase of DO 2 , VO 2 and O 2 ER (oxygen extraction ratio) occurred after infusion of NAC.…”

Alterations in the functions of the reticuloendothelial and protease-antiprotease systems after intraperitoneal injection of zymosan in rats

“…It is a well known antioxidant with multiple functions (24), and is mainly metabolised to cysteine (a precursor in the biosynthesis of glutathione); it increases glutathione and sulfhydryl concentrations, and reduces hydrogen peroxide-dependent injury by inactivating the hypochlorous acid and hydroxyl radicals formed by hydrogen peroxide (2). NAC may also have beneficial effects, such as decreasing neutrophil-aggregating activity and increasing cardiac output and oxygen delivery (25). The reducing effect of NAC on production of tumour necrosis factor (TNF) is most likely caused by a decreased release of oxygen free radicals (29).…”