Observation on the ultrastructure morphology of HeLa cells treated with ethanol: Statistical analysis
Autor: | Humberto Munoz Barona, James P. Geaghan, Masami Yoshimura, Shaomian Yao, Fakhri Al-Bagdadi, Eduardo Martinez-Ceballos, Matthew J. Young |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Ethanol Phospholipid Oxidative phosphorylation Mitochondrion Biology Mitochondria Pathology and Forensic Medicine Cell biology 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology chemistry Structural Biology Apoptosis Mitochondrial Membranes Organelle Membrane fluidity Ultrastructure Humans Mitochondrial Swelling Lipid bilayer Cell Shape HeLa Cells |
Zdroj: | Ultrastructural Pathology. 40:324-332 |
ISSN: | 1521-0758 0191-3123 |
Popis: | It is estimated that 5.9% of all human deaths are attributable to alcohol consumption and that the harmful use of ethanol ranks among the top five risk factors for causing disease, disability, and death worldwide. Ethanol is known to disrupt phospholipid packing and promote membrane hemifusion at lipid bilayers. With the exception of mitochondria involved in hormone synthesis, the sterol content of mitochondrial membranes is low. As membranes that are low in cholesterol have increased membrane fluidity and are the most easily disordered by ethanol, we hypothesize that mitochondria are sensitive targets for ethanol damage. HeLa cells were exposed to 50 mM ethanol and the direct effects of ethanol on cellular ultrastructure were examined utilizing transmission electron microscopy. Our ultramicroscopic analysis revealed that cells exposed to ethanol harbor fewer incidence of apoptotic morphology; however, significant alterations to mitochondria and to nuclei occurred. We observed statistical increases in the amount of irregular cells and cells with multiple nuclei, nuclei harboring indentations, and nuclei with multiple nucleolus-like bodies. Indeed, our analysis revealed that mitochondrial damage is the most extensive type of cellular damage. Rupturing of cristae was the most prominent damage followed by mitochondrial swelling. Ethanol exposure also resulted in increased amounts of mitochondrial rupturing, organelles with linked membranes, and mitochondria localizing to indentations of nuclear membranes. We theorize that these alterations could contribute to cellular defects in oxidative phosphorylation and, by extension, the inability to generate regular levels of cellular adenosine triphosphate. |
Databáze: | OpenAIRE |
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