Abstract
BackgroundThe radiation-induced energy metabolism dysfunction related to injury and radiation doses is largely elusive. The purpose of this study is to investigate the early response of energy metabolism in small intestinal tissue and its correlation with pathologic lesion after total body X-ray irradiation (TBI) in Tibet minipigs.Methods and Results30 Tibet minipigs were assigned into 6 groups including 5 experimental groups and one control group with 6 animals each group. The minipigs in these experimental groups were subjected to a TBI of 2, 5, 8, 11, and 14 Gy, respectively. Small intestine tissues were collected at 24 h following X-ray exposure and analyzed by histology and high performance liquid chromatography (HPLC). DNA contents in this tissue were also examined. Irradiation causes pathologic lesions and mitochondrial abnormalities. The Deoxyribonucleic acid (DNA) content-corrected and uncorrected adenosine-triphosphate (ATP) and total adenine nucleotides (TAN) were significantly reduced in a dose-dependent manner by 2–8 Gy exposure, and no further reduction was observed over 8 Gy.ConclusionTBI induced injury is highly dependent on the irradiation dosage in small intestine and inversely correlates with the energy metabolism, with its reduction potentially indicating the severity of injury.
Highlights
Radiation-induced mitochondria damage has been extensively studied in the past decade
total body X-ray irradiation (TBI) induced injury is highly dependent on the irradiation dosage in small intestine and inversely correlates with the energy metabolism, with its reduction potentially indicating the severity of injury
Mitochondria are susceptible to ionizing radiation because of radiation-induced reactive oxygen species (ROS) overproduction and mitochondrial deoxyribonucleic acid damage [1,2]
Summary
Radiation-induced mitochondria damage has been extensively studied in the past decade. Following irradiation exposure, enhanced ROS production leads to mitochondrial dysfunction through the disruption of electron flow and mtDNA, subsequently causes cell apoptosis [3]. It is largely unknown whether bioenergetic failure is associated with radiation-induced organ injury. Bioenergetic failure induced by mitochondrial dysfunction may play a role in organ injury, including small intestinal tissue. The purpose of this study is to investigate the early response of energy metabolism in small intestinal tissue and its correlation with pathologic lesion after total body X-ray irradiation (TBI) in Tibet minipigs
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