Transmission electron microscopy of the liver mitochondria of N‐Nitrosodibutylamine‐treated mice

N‐Nitrosodibutylamine (DBN) has been found in a wide variety of products because of the nitrosation of amines present in these products. An extensive series of synthesis and carcinogenicity studies of various compounds related to DBN and its metabolites have revealed that they have markedly different carcinogenic effects. The role of mitochondria in disease has been found to be expanded beyond the respiratory chain, as defects in additional mitochondrial functions and behaviors have been linked to cancer, metabolic disorders, and many neurodegenerative diseases, such as Alzheimer's, Parkinson's, and Huntington's disease (Nunnari & Suomalainen (2012) Cell, 148, 1145–1159). The sample preparation was performed using the protocol standardized by Sophisticated Analytical Instrumentation Facility (SAIF) laboratory in NEHU. The prepared sample was then mounted and observed under the transmission electron microscope model JEM‐100 CC II. The micrographs obtained from transmission electron microscopy (TEM) at various magnifications 2,000, 5,000, and 12,000× from DBN‐treated mice showed significant changes. Mitochondria showed variability in number, size, and shape. This significant alteration in the morphology and population of liver mitochondria observed in DBN‐treated animals in comparison to that of the age‐matched normal control mice provide a unique potential for the use of mitochondria as markers for the early detection for the treatment of liver cancer. Effect of DBN on liver mitochondria. DBN in 5% ethanol when administration intravenously (10 mg/kg body weight) at weekly interval for 12–16 weeks induces hepatocarcinogenesis in Swiss albino mice. Assays of marker enzyme activities, namely GGT, AChE, and GST and the histological examination of liver in DBN‐exposed animals signify cellular transformation. The observed alterations in LFTs clearly indicate hepatic dysfunction and damage to liver, which is caused by DBN treatment in mice. Significant alteration in the morphology and population of liver mitochondria was observed in DBN‐treated animals in comparison to that of the age‐matched normal control mice. Drastic distortion in shape and size was found in the mitochondria of DBN‐treated mice. Our study revealed that DBN not only makes alterations in hepatocytes but also induces significant alterations in the morphology and functional aspects of liver mitochondria. These changes in mitochondria provide a unique potential for the use of mitochondria as marker