Abstract
BackgroundHepatic iron overload has been implicated in many liver diseases; however, whether it is involved in clonorchiasis remains unknown. The purpose of this study is to investigate whether Clonorchis sinensis (C. sinensis) infection causes hepatic iron overload, analyze the relationship between the iron overload and associated cell apoptosis, so as to determine the role of excess iron plays in C. sinensis-induced liver injury.MethodsThe Perls’ Prussian staining and atomic absorption spectrometry methods were used to investigate the iron overload in hepatic sections of wistar rats and patients infected with C. sinensis. The hepatic apoptosis was detected by transferase uridyl nick end labeling (TUNEL) methods. Spearman analysis was used for determining the correlation of the histological hepatic iron index and the apoptotic index.ResultsBlue iron particles were deposited mainly in the hepatocytes, Kupffer cells and endothelial cells, around the liver portal and central vein area of both patients and rats. The total iron score was found to be higher in the infected groups than the respective control from 8 weeks. The hepatic iron concentration was also significantly higher in treatment groups than in control rats from 8 weeks. The hepatocyte apoptosis was found to be significantly higher in the portal area of the liver tissue and around the central vein. However, spearman’s rank correlation coefficient revealed that there was a mildly negative correlation between the iron index and hepatocyte apoptosis.ConclusionsThis present study confirmed that hepatic iron overload was found during C. sinensis infection. This suggests that iron overload may be associated with hepatocyte apoptosis and involved in liver injury during C. sinensis infection. Further studies are needed to investigate the molecular mechanism involved here.
Highlights
Hepatic iron overload has been implicated in many liver diseases; whether it is involved in clonorchiasis remains unknown
Deposits were found in liver tissue from patients infected with C. sinensis, whereas none were recorded in normal controls (Fig. 1A)
We speculated that liver iron overload in C. sinensis infection may be associated with abnormal iron metabolism, increasing the amount of iron absorbed, and with elevated levels of iron being released from damaged hepatocytes or through the phagocytosis of damaged, iron-loaded hepatocytes by Kupffer cells
Summary
Hepatic iron overload has been implicated in many liver diseases; whether it is involved in clonorchiasis remains unknown. The purpose of this study is to investigate whether Clonorchis sinensis (C. sinensis) infection causes hepatic iron overload, analyze the relationship between the iron overload and associated cell apoptosis, so as to determine the role of excess iron plays in C. sinensis-induced liver injury. Clonorchiasis, caused by Clonorchis sinensis (C. sinensis), is an important food-borne parasitic disease. It is estimated that 35 million people are infected worldwide, including approximately 15 million people in China [1]. Humans become infected by ingesting freshwater fish containing C. sinensis metacercariae. Clonorchiasis remains a significant public health problem in China. Heavy or long-term chronic infections provoke epithelial hyperplasia, periductal fibrosis, cholelithiases, cholecystitis, hepatic fibrosis, and even cholangiocarcinoma [2].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
