Biochemical disorders in the thyroid gland in rats with hyperhomocysteinemia
DOI:
https://doi.org/10.15419/bmrat.v9i5.740Keywords:
endogenous intoxication, hyperhomocysteinemia, inflammation, proteolysis, thyroid glandAbstract
Background: In recent years, significant progress has been made in elucidating the mechanisms of development of complications associated with hyperhomocysteinemia (HC), but little is known about the disorders in the thyroid gland. This study aimed to determine the levels of low-molecularweight degradation products and peptides in the thyroid gland of rats with HC. In addition, markers of inflammation and the proteolytic state were also assessed.
Methods: HC was induced by intragastric administration of DL-homocysteine thiolactone (100 mg.kg-1 of body weight) to albino non-linear male rats. The levels of low-molecular-weight substances (LMWS) of various nature were detected at wavelengths of 254 and 280 nm. The levels of MMP-2 and cytokine profiles were detected by enzyme-linked immunosorbent assay. The protein composition and the presence of active enzymes were assessed by SDS-polyacrylamide gel electrophoresis and zymography, respectively.
Results: Obtained results can indicate the enhancement of catabolic reactions, confirmed by the accumulation of LMWS in the blood and thyroid gland of the rats with HC. The state of inflammation, evidenced by the significantly increased pro-inflammatory cytokines, was also revealed. HC was accompanied by the activation of proteolysis, expressed by an increase in overall proteolytic activity, the level of MMP-2, and changes in protein profile. Proteins accumulated with a molecular weight of less than 30 kDa simultaneously with the decrease in the level of high-molecular-weight proteins.
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Copyright The Author(s) 2017. This article is published with open access by BioMedPress. This article is distributed under the terms of the Creative Commons Attribution License (CC-BY 4.0) which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.