scholarly journals Acute liver injury associated with Oxyfluorfen toxicity

2021 ◽  
Vol 9 ◽  
pp. 2050313X2110004
Author(s):  
Selladurai Pirasath ◽  
Ayshanie Gayanthika Samasundara Mudiyanselage ◽  
Manosha Harshani Seneviratne
Keyword(s):  
Sri Lanka ◽  
Liver Injury ◽  
Young Woman ◽  
Broad Spectrum ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Toxic Dose ◽  
Acute Hepatic Injury ◽  
Haem Biosynthesis ◽  
Spectrum Control

Oxyfluorfen is a phenoxyphenyl-type herbicide which is used for broad-spectrum control of broadleaf and grassy weeds. Ingestion of toxic dose of oxyfluorfen can be fatal among animals. However, toxicity to humans are rare in literature. The alterations in haem biosynthesis (anaemia) and in liver are the primary toxic effects. There are no specific antidotes and none of the current treatments have proven efficacious till date. Therefore, prevention needs to be the utmost priority, and on exposure, aggressive decontamination should be initiated. Herein, we described an oxyfluorfen toxicity with acute hepatic injury in a young woman who presented with a deliberate self-harming with an oxyfluorfen poisoning in Sri Lanka.

Systemic and hepatic hemodynamic changes in acute liver injury

1997 ◽  
Vol 272 (3) ◽  
pp. G617-G625 ◽  
Author(s):  
A. J. Makin ◽  
R. D. Hughes ◽  
R. Williams
Keyword(s):  
Blood Flow ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Venous Blood ◽  
Marked Change ◽  
Arterial Blood Flow ◽  
Venous Flow ◽  
Subsequent Increase ◽  
Arterial Blood

Systemic and hepatic circulatory changes were studied in rats over the course of acute liver injury. Hepatic injury was induced by intraperitoneal injection of D-galactosamine (1.1 g/kg), and systemic and hepatic hemodynamics were measured over a 72-h period using a radioactive microsphere technique with direct measurement of arterial, portal venous, and hepatic venous blood oxygen content. Cardiac output increased to a maximum at 48 h, producing a marked increase (450%) in hepatic arterial blood flow so that it became the dominant supply of oxygen at the time of maximal hepatic injury. A subsequent increase in portal venous flow resulted in an overall increase in total hepatic blood flow of 500%. At this point the oxygen delivery by the hepatic arterial and portal venous systems was equal. These circulatory changes returned to control values by 72 h with recovery of liver function. These results demonstrate the development of a hyperdynamic circulation and a marked change in the normal relationship between portal venous and hepatic arterial blood flows that occur during hepatic injury.

scholarly journals Ascites management by cell-free concentrated ascites reinfusion therapy during recovery from drug-induced acute liver injury: a case report

2020 ◽  
Vol 14 (1) ◽  
Author(s):  
Koya Yasuda ◽  
Mea Asou ◽  
Tomohiko Asakawa ◽  
Makoto Araki
Keyword(s):  
Liver Injury ◽  
Liver Regeneration ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Artery Bypass ◽  
Severe Disease ◽  
International Normalized Ratio ◽  
Cardiac Complications ◽  
Massive Ascites ◽  
Drug Induced

Abstract Background The symptoms of drug-induced hepatic injury are manifold; however, the presence of ascites indicates a severe disease condition. The rapid accumulation of ascites is distressing and requires palliative treatment. Because many cases are addressed by repeated large-volume paracentesis, often resulting in impairment due to protein and electrolyte loss, a different approach is required. Case presentation A 61-year-old Japanese man on maintenance dialysis was admitted to our hospital with acute liver injury. Our patient was diagnosed as having drug-induced liver injury due to warfarin or diltiazem, which started immediately after coronary artery bypass grafting 7 months previously. One month after admission, our patient’s hepatic encephalopathy remained grade 1 and his prothrombin time international normalized ratio was maintained at < 1.5. However, the liver was markedly atrophied with massive ascites. Although liver transplantation was desired, he was considered unfit for transplantation because of his renal and cardiac complications. Therefore, we devised a strategy to manage the massive ascites with cell-free concentrated ascites reinfusion therapy while awaiting liver regeneration. At first, cell-free concentrated ascites reinfusion therapy was required frequently because ascites accumulated rapidly. But the fluid retention interval was gradually extended as intended, and cell-free concentrated ascites reinfusion therapy was withdrawn after 8 months. During that time, the size of his liver increased from 1419 cm3 to 1587 cm3 on computed tomography. Conclusions Cell-free concentrated ascites reinfusion therapy is an apheresis therapy in which ascites are collected aseptically by paracentesis, concentrated, and then reinfused intravenously. This treatment has the advantage of preserving nutrition by reusing the fluid. Previously, cell-free concentrated ascites reinfusion therapy was used only for the management of ascites in patients with cirrhosis or carcinomatous peritonitis. This case suggests that palliation and maintenance of nutritional status with cell-free concentrated ascites reinfusion therapy may be useful as an adjunct to liver regeneration in drug-induced hepatic injury.

Capsaicin, the pungent principle of peppers, ameliorates alcohol-induced acute liver injury in mice via modulation of matrix metalloproteinases

2018 ◽  
Vol 96 (4) ◽  
pp. 419-427 ◽  
Author(s):  
Meghana Koneru ◽  
Bidya Dhar Sahu ◽  
Salma Mukhtar Mir ◽  
Halley Gora Ravuri ◽  
Madhusudana Kuncha ◽  
...  
Keyword(s):  
Liver Injury ◽  
Matrix Metalloproteinases ◽  
Alcohol Intake ◽  
Hepatic Injury ◽  
Dietary Intervention ◽  
Acute Liver Injury ◽  
Experimental Period ◽  
Hepatic Tissue ◽  
Protein Levels ◽  
Dietary Antioxidant

Alcohol, the most common cause for hepatic injury, may further deteriorate the hepatic tissue when left unattended. Capsaicin, the pungent principle of chilli peppers, possesses antioxidant and anti-inflammatory properties and is a proven dietary antioxidant in various ailments. However, its role in alcohol-induced hepatic injury is unclear. In this study, we investigated the effects of capsaicin on the hepatic tissue of mice treated with alcohol. Acute liver injury was induced in mice by oral gavage of 5 doses of 10 mL/kg of 50% ethyl alcohol at an interval of 12 h. The tissue antioxidant levels along with the mitochondrial functional parameters and matrix metalloproteinase levels were evaluated in the hepatic tissues of mice following alcohol challenge. The results showed that alcohol intake significantly attenuated the hepatic antioxidant levels and mitochondrial function. These changes were accompanied by enhanced serum hepatic injury markers and matrix metalloproteinases. However, capsaicin treatment (10 and 20 mg/kg, oral) throughout the experimental period caused a drastic improvement in the hepatic tissue of the alcohol-treated mice, reflected by the normalization of hepatic enzyme and protein levels along with restored histological alterations. These results indicate that capsaicin, as a dietary intervention, may prevent alcohol-induced acute liver injury.

scholarly journals Patchouli oil isolated from the leaves of Pogostemon cablin ameliorates ethanol-induced acute liver injury in rats via inhibition of oxidative stress and lipid accumulation

RSC Advances ◽  
2018 ◽  
Vol 8 (43) ◽  
pp. 24399-24410 ◽  
Author(s):  
Qiong-Hui Huang ◽  
Xue Wu ◽  
Xiao-Hong Chen ◽  
Jia-Zhen Wu ◽  
Zi-Ren Su ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alcohol Consumption ◽  
Liver Injury ◽  
Lipid Accumulation ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Metabolic Disturbance ◽  
Excessive Alcohol Consumption ◽  
Pogostemon Cablin ◽  
Excessive Alcohol

Excessive alcohol consumption can cause serious hepatic injury which is associated with oxidative stress and fatty metabolic disturbance.

Polysaccharides from Enteromorpha prolifera protect against carbon tetrachloride-induced acute liver injury in mice via activation of Nrf2/HO-1 signaling, and suppression of oxidative stress, inflammation and apoptosis

2020 ◽  
Vol 11 (5) ◽  
pp. 4485-4498
Author(s):  
Fuchuan Guo ◽  
Xinyun Zhuang ◽  
Mengyuan Han ◽  
Wenting Lin
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Reactive Intermediates ◽  
Enteromorpha Prolifera ◽  
Hepatic Oxidative Stress

EPP protected against hepatic injury induced by CCl4-derived reactive intermediates through the suppression of hepatic oxidative stress, inflammation, and apoptosis.

scholarly journals Allogenic Adipose Tissue-Derived Mesenchymal Stem Cells Ameliorate Acute Hepatic Injury in Dogs

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Takahiro Teshima ◽  
Hirotaka Matsumoto ◽  
Masaki Michishita ◽  
Akito Matsuoka ◽  
Maika Shiba ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Adipose Tissue ◽  
Veterinary Medicine ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Splenic Vein ◽  
Therapeutic Effects ◽  
Cell Based Therapy ◽  
Acute Hepatic Injury

Adipose tissue-derived mesenchymal stem cells (AT-MSCs) are an attractive source for cell-based therapy of some diseases, including acute and chronic liver failure, in not only human medicine but also veterinary medicine. However, in veterinary medicine, no studies have reported the effects of AT-MSCs on liver injury in dogs. The purpose of this study was to investigate the effects of allogenic AT-MSCs on acute liver injury by carbon tetrachloride in dogs and to compare the therapeutic effects of AT-MSCs transplanted via the peripheral vein (PV) or splenic vein (SV). After transplantation of AT-MSCs through the PV or SV, serum liver enzymes were decreased significantly, and SV injection was more effective compared with PV injection. By comparing the number of engrafted AT-MSCs in the liver, SV injection was significantly more effective than PV injection. mRNA expression levels of proinflammatory cytokines, such as IL-1, IL-6, IL-8, and IFNγ, in the liver were decreased significantly, but those of anti-inflammatory cytokines, such as IL-4 and IL-10, HGF, and VEGFA, were significantly increased after the first AT-MSC injection. These findings suggest that allogenic AT-MSCs injected via the PV or SV ameliorate acute hepatic injury in dogs, and AT-MSCs injected via the SV provide more effective improvement.

scholarly journals Aloperine attenuates carbon tetrachloride-induced mouse hepatic injury via Nrf2/HO-1 pathway

2020 ◽  
Vol 19 (5) ◽  
pp. 983-988
Author(s):  
Rui Xiong ◽  
Shuzhong Shan ◽  
Xiaoming Wang ◽  
Xiaowen Zhang ◽  
Haixia Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Control Group ◽  
Histopathological Analysis ◽  
Dependent Manner ◽  
Oxidative Stress Biomarkers ◽  
Cox 2

Purpose: To investigate whether aloperine pretreatment ameliorates acute liver injury in carbon tetrachloride (CCl4)-treated mice.Methods: Mice were injected with CCl4 and orally administered aloperine. Blood samples and liver tissues were used for histopathological and biochemical analyses, respectively. Protein expression levels were determined by western blotting.Results: Histopathological analysis indicate that aloperine pretreatment significantly alleviated CCl4- induced mouse hepatic injury. CCl4 treatment induced the upregulation of aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine amino transferase (ALT), and total bilirubin (p < 0.05). However, these alterations were significantly inhibited by aloperine treatment. Moreover, aloperine pretreatment markedly decreased (p < 0.05) the CCl4-induced expression of oxidative stress biomarkers, including malondrialdeline (MDA), glutathione (GSH), catalase (CAT), and  superoxide dismutase (SOD). Compared to the control group, the protein levels of Nrf2, HO-1, iNOS, and COX-2 were significantly increased in the CCl4 group, while Nrf2 and HO-1 were upregulated. Furthermore, iNOS and COX-2 were downregulated in mouse liver in CCl4 + aloperine group compared to CCl4 group in a concentration-dependent manner (p < 0.05).Conclusion: Aloperine pretreatment appears to markedly upregulate Nrf2 and HO-1 and downregulate iNOS and COX-2 to suppress hepatic injury in mice. Thus, aloperine is a promising treatment for acute liver injury. Keywords: Hepatic injury, Aloperine, Oxidative stress, Nrf2/HO-1 pathway

Suppression of acute hepatic injury by a synthetic prostacyclin agonist through hepatocyte growth factor expression

2012 ◽  
Vol 302 (4) ◽  
pp. G420-G429 ◽  
Author(s):  
Qing Xu ◽  
Mizuho Nakayama ◽  
Yoshinori Suzuki ◽  
Katsuya Sakai ◽  
Takahiro Nakamura ◽  
...  
Keyword(s):  
Growth Factor ◽  
Liver Injury ◽  
Hepatocyte Growth Factor ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Protective Action ◽  
Liver Cells ◽  
Cyclooxygenase 2 ◽  
Peroral Administration ◽  
Hepatocyte Growth

Previous studies have demonstrated that mice disrupted with the cyclooxygenase-2 gene showed much more severe liver damage compared with wild-type mice after liver injury, and prostaglandins (PGs) such as PGE1/2 and PGI2 have decreased hepatic injury, but the mechanisms by which prostaglandins exhibit protective action on the liver have yet to be addressed. In the present study, we investigated the mechanism of the protective action of PGI2 using the synthetic IP receptor agonist ONO-1301. In primary cultures of hepatocytes and nonparenchymal liver cells, ONO-1301 did not show protective action directly on hepatocytes, whereas it stimulated expression of hepatocyte growth factor (HGF) in nonparenchymal liver cells. In mice, peroral administration of ONO-1301 increased hepatic gene expression and protein levels of HGF. Injections of CCl4 induced acute liver injury in mice, but the onset of acute liver injury was strongly suppressed by administration of ONO-1301. The increases in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) by CCl4 were suppressed by 10 mg/kg ONO-1301 to 39.4 and 33.6%, respectively. When neutralizing antibody against HGF was administered with ONO-1301 and CCl4, the decreases by ONO-1301 in serum ALT and AST, apoptotic liver cells, and expansion of necrotic areas in liver tissue were strongly reversed by neutralization of endogenous HGF. These results indicate that ONO-1301 increases expression of HGF and that hepatoprotective action of ONO-1301 in CCl4-induced liver injury may be attributable to its activity to induce expression of HGF, at least in part. The potential for involvement of HGF-Met-mediated signaling in the hepatotrophic action of endogenous prostaglandins generated by injury-dependent cyclooxygenase-2 induction is considerable.

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