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We investigated apoptotic effects and changes in glucose-6-phosphate dehydrogenase (G6PD) enzyme activity in liver and gill tissues of fish exposed to chlorpyrifos. Three different chlorpyrifos doses (2.25, 4.5 and 6.75 μg/L) were administrated to rainbow trout at different time intervals (24, 48, 72 and 96 h). Acute exposure to chlorpyrifos showed time dependent decrease in G6PD enzyme activity at all concentrations (p < 0.05). Immunohistochemical results showed that chlorpyrifos caused mucous cell loss in gill tissue and apoptosis via caspase-3 activation in fish. The present study suggested that chlorpyrifos inhibits G6PD enzyme and causes mucous cell loss in gill and apoptosis in gill and liver tissues.
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http://dx.doi.org/10.1016/j.tice.2014.09.001 | DOI Listing |
Talanta
August 2025
Department of Molecular Tropical Medicine and Genetics, Faculty of Tropical Medicine, Mahidol University, Bangkok, 10400, Thailand. Electronic address:
A rapid and automated determination of nicotinamide adenine dinucleotide phosphate (NADPH) is proposed and applied to the evaluation of glucose-6-phosphate dehydrogenase (G6PD) deficiency in real samples. To this end, a sequential injection analyzer with electrochemical detection (SIA-ECD) is proposed with 0.1 mol L Tris-HCl (pH 8.
View Article and Find Full Text PDFMol Biol Rep
September 2025
Department of Scientific Management, First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, Anhui, China.
Background: Malignant tumors are characterized by their reliance on hyperactive glycolysis (Warburg effect), marked by increased glucose uptake, lactate secretion, and preferential glucose flux into glycolysis and the pentose phosphate pathway (PPP). These metabolic shifts provide energy, biosynthetic precursors, and maintain redox balance, supporting tumor proliferation. However, the regulatory crosstalk between glycolysis and PPP remains poorly understood.
View Article and Find Full Text PDFChildren (Basel)
August 2025
Department of Obstetrics and Gynecology, RAK College of Medical Sciences, RAK Medical and Health Sciences University, Ras Al Khaimah P.O. Box 11172, United Arab Emirates.
Autism spectrum disorder (ASD) is a complex neurodevelopmental disease of multifactorial etiologies, manifesting as persistent challenges in social interactions, restrictive interests, and repetitive behaviors. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzymopathy affecting red blood cell function. Although G6PD enzyme deficiency is known for its role in hemolytic anemia, emerging studies have suggested a potential association between G6PD deficiency and neurodegenerative and neurodevelopmental disorders, including autism.
View Article and Find Full Text PDFbioRxiv
August 2025
University of Washington, Department of Genome Sciences, Seattle, WA, 98195, USA.
G6PD deficiency is the most common enzyme deficiency worldwide, and increases the likelihood of adverse reactions to certain drugs and foods. Identifying people at risk is challenging, since most are asymptomatic until they encounter a trigger. This is further complicated since over 60% of 1,548 known genetic variants in are variants of uncertain significance and thus cannot guide drug prescribing and dosing.
View Article and Find Full Text PDFInt Med Case Rep J
August 2025
Emergency Department, Tamale West Hospital, Tamale, Ghana.
Glucose-6-phosphate dehydrogenase (G6PD) deficiency, a sex-linked chromosomal disorder, is the most common enzymopathy in humans. This enzyme, which protects red blood cells, when deficient, predisposes individuals to hemolysis under oxidative stress. Several chemicals and drugs have been commonly known to cause hemolysis in G6PD deficiency.
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