The influence of sterol metabolism upon mutagenesis in Drosophila melanogaster was investigated using ecological-genetic yeast - drosophila system. Sterol deficiency in the organism of Drosophila was caused by using the strain of Saccharomyces cerevisiae 9-2P712 with a mutation in the nysr1 locus which blocks synthesis of ergosterol as a nutrition substrate for flies. It was concluded that maintenance of females on the mutant yeast strain causes an increase of radiation-induced X-chromosome loss in mature oocytes. Resistance of oocytes to X-ray irradiation is restored, reaching the control level, when 0,1% cholesterol solution in 10% ethanol is added to the yeast biomass. The possible membrane and hormonal mechanisms of elevation of induced aneuploidy and the role of sterol metabolism in ensuring resistance of insects to damaging factors are discussed.

Download full-text PDF

Source

Publication Analysis

Top Keywords

sterol metabolism
12
drosophila melanogaster
8
[effect sterol
4
metabolism yeast-drosophila
4
yeast-drosophila system
4
system frequency
4
frequency radiation-induced
4
radiation-induced aneuploidy
4
drosophila
4
aneuploidy drosophila
4

Similar Publications

Background: Early neurological deterioration (END) is a critical determinant influencing the short-term prognosis of acute ischemic stroke (AIS) patients and is associated with increased mortality rates among hospitalized individuals. AIS frequently coexists with coronary heart disease (CHD), complicating treatment and leading to more severe symptoms and worse outcomes. Shared risk factors between CHD and AIS, especially elevated low-density lipoprotein cholesterol (LDL-C), contribute to atherosclerosis and inflammation, which worsen brain tissue damage.

View Article and Find Full Text PDF

NPC1 controls TGFBR1 stability in a cholesterol transport-independent manner and promotes hepatocellular carcinoma progression.

Nat Commun

January 2025

State Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing), Beijing Proteome Research Center, Beijing Institute of Lifeomics, Beijing, China.

Niemann-Pick disease type C protein 1 (NPC1), classically associated with cholesterol transport and viral entry, has an emerging role in cancer biology. Here, we demonstrate that knockout of Npc1 in hepatocytes attenuates hepatocellular carcinoma (HCC) progression in both DEN (diethylnitrosamine)-CCl induced and MYC-driven HCC mouse models. Mechanistically, NPC1 significantly promotes HCC progression by modulating the TGF-β pathway, independent of its traditional role in cholesterol transport.

View Article and Find Full Text PDF

A new fusidic acid-loaded hydrogel film was prepared via the solvent casting technique using alginate and Aloe vera. The hydrogel films were optimized using different ratios of sodium alginate, Aloe vera, and glycerin. The films containing 10% glycerin (w/w of alginate) exhibited the best appearance.

View Article and Find Full Text PDF

Background And Purpose: Cerebrotendinous xanthomatosis (CTX) is a rare autosomal recessive lipid storage disease characterized by abnormal bile acid synthesis. It often presents with systemic and neurological manifestations; however, atypical presentations can lead to significant diagnostic challenges. This case report highlights the diagnostic complexities and management considerations in a patient with an uncommon presentation of CTX.

View Article and Find Full Text PDF

Food-derived components with physiological effects have been attracting attention in recent years, and studies have comprehensively analyzed these components. In this study, we sought to identify food components with functional properties for the prevention and improvement of metabolic syndrome. We performed a luciferase reporter assay using fatty acid synthase (FAS) and low-density lipoprotein receptor (LDL) receptor gene promoters.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!