MULTI-ORGAN METABOLIC PERTURBATION STUDY OF DEXTRAN SULFATE SODIUM-INDUCED ULCERATIVE COLITIS USING GLYCOLYTIC AND MITOCHONDRIAL METABOLIZING ENZYMES AS INDICES
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Ulcerative colitis is an inflammatory bowel disease, which includes chronic inflammation of the
gastrointestinal tract. Recent studies have suggested that the etiology of inflammatory bowel disease
is multifactorial, resulting from the interplay of immunological, molecular, genetic, microbial, diet,
drug use-related, and environmental factors. This study was designed to investigate multiple organ
toxicity of Dextran sulfate sodium-induced (DSS) ulcerative colitis using glycolytic and
mitochondrial metabolizing enzymes as indices Twelve mice were divided into two groups of six
mice each. Group A (Control) received normal drinking water while group B was fed with 2.5% DSS
for 7 days in their drinking water, and the dextran sulfate sodium solution was replenished daily. The
liver, kidney, colon, spleen was excised from the mice after the last administration of DSS, glycolytic
and mitochondrial metabolizing enzymes were assessed in all the organs and lymphocytes.
Activities of glycolytic enzymes lactate dehydrogenase and NADase were down-regulated in all the
organs. Hepatic hexokinase activity significantly reduced as opposed to the increase observed in
other organs, while aldolase activities were up-regulated in all the organs. Furthermore, DSS
administration caused perturbation in the activities of mitochondrial metabolizing enzymes in all the
organs. Activities of succinate dehydrogenase, malate dehydrogenase, Combined Complexes I+III,
II+III, and IV were down-regulated. All observations are relative to control. ata from this study
demonstrated that administration of DSS induced ulcerative colitis which invariably perturbs the
glycolytic enzymes while mitochondrial metabolizing enzymes are down-regulated leading to
decreased energy availability for cellular processes during ulcerative colitis pathological condition.
提供机构:
Journal of Experimental Research
创建时间:
2024-03-28



