Publications by authors named "A C Roginski"
Disturbances in mitochondrial bioenergetics and control quality and unbalanced redox homeostasis in the liver of a mouse model of mucopolysaccharidosis type II.
Mol Cell Biochem
January 2025
Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is a lysosomal storage disease caused by mutations in the gene encoding the enzyme iduronate 2-sulfatase (IDS) and biochemically characterized by the accumulation of glycosaminoglycans (GAGs) in different tissues. It is a multisystemic disorder that presents liver abnormalities, the pathophysiology of which is not yet established. In the present study, we evaluated bioenergetics, redox homeostasis, and mitochondrial dynamics in the liver of 6-month-old MPS II mice (IDS).
View Article and Find Full Text PDFBackground: Nanoencapsulation has opened promising fields of innovation for pesticides. Conventional pesticides can cause side effects on plant metabolism. To date, the effect of nanoencapsulated pesticides on plant phenolic contents has not been reported.
View Article and Find Full Text PDFMitochondrial dysfunction, oxidative stress, ER stress and mitochondria-ER crosstalk alterations in a chemical rat model of Huntington's disease: Potential benefits of bezafibrate.
Toxicol Lett
May 2023
Article Synopsis
- - The study examined how 3-nitropropionic acid (3-NP), a chemical linked to Huntington's disease, affects redox homeostasis, mitochondrial function, and communication between mitochondria and the endoplasmic reticulum (ER) in rat brains over different time points.
- - 3-NP was found to disrupt redox balance by increasing harmful malondialdehyde levels and decreasing important antioxidants like glutathione, ultimately impairing mitochondrial respiration and enzyme activities critical for energy production.
- - Treatment with bezafibrate showed promise in counteracting these negative effects by stabilizing antioxidant enzyme activities and reducing mitochondrial dysfunction, suggesting it could be beneficial as a complementary therapy for Huntington's disease.
Unlabelled: Metabolic dysfunction-associated fatty liver disease (MAFLD) has gained worldwide attention as a public health problem. Nonetheless, lack of enough mechanistic knowledge restrains effective treatments. It is known that thyroid hormone triiodothyronine (T3) regulates hepatic lipid metabolism, and mitochondrial function.
View Article and Find Full Text PDFDisruption of mitochondrial bioenergetics and calcium homeostasis by phytanic acid in the heart: Potential relevance for the cardiomyopathy in Refsum disease.
Biochim Biophys Acta Bioenerg
April 2023
Article Synopsis
- Refsum disease is an inherited disorder that severely affects an enzyme needed to break down a fatty acid called phytanic acid, leading to serious heart problems.
- Research showed that high levels of phytanic acid can damage mitochondria in heart cells, disrupting their function and leading to decreased energy production and increased cell death.
- Affected cardiac cells exhibited reduced mitochondrial performance and calcium retention, suggesting that phytanic acid contributes to the heart issues seen in patients with Refsum disease.