Disease relevance of Fluazifop

• Short-term treatment of rats with fluazifop resulted in hepatomegaly due to time dependent proliferation of smooth endoplasmic reticulum (SER) and peroxisomes [1].
• Thus, we can conclude that fluazifop produces in male Wistar rats hepatomegaly due to cellular hypertrophy [1].
• Fluazifop was administered orally to male Wistar rats at increasing doses from 5.6 to 891 mg/kg body weight per day for 1, 2, 4, 7 and 14 consecutive days and peroxisome proliferation, induction of some peroxisome-associated enzymes and mitogenesis (S-phase, M-phase and percentage of binucleated hepatocytes) were studied [1].

High impact information on Fluazifop

• Results from four different types of experiment show that this inhibition is due to an action of fluazifop on acetyl-CoA carboxylase and not on fatty acid synthetase [2].
• Fluazifop-butyl was hydrolysed to fluazifop by rat liver (Vmax mumol/min/g microsomes 6.2 +/- 0.4; cytosol 6.84 +/- 0.85), lung (Vmax microsomes 0.38 +/- 0.1; cytosol 1.5 +/- 0.32) and skin (Vmax microsomes 0.02 +/- 0.0015; cytosol 0.4 +/- 0.06) and by plasma (Vmax mumol/min/mL 5.8 +/- 0.48) and red blood cells (Vmax 0.03 +/- 0.015) [3].
• Hepatocellular peroxisome proliferation and DNA synthesis in Wistar rats treated with herbicide fluazifop [1].
• In contrast to other PPs fluazifop induced low rate of rcplicative DNA synthesis and did not affect mitoses (M-phase) [1].
• 5. When six volunteers were given a daily dermal dose of the 0.5% formulation for five consecutive days, the plasma and urinary excretion kinetics of fluazifop could be accurately predicted by simple mathematical extrapolation of the kinetic data from the single exposure study at the equivalent daily dose [4].

Biological context of Fluazifop

• Liquid chromatography with amperometric detection (LC/AD) is used to determine fluazifop acid produced from the metabolism or base hydrolysis of fluazifop-butyl in soybeans and soybean oil [5].

Anatomical context of Fluazifop

• The aim of this study was to determine the effect of herbicide fluazifop, on the early occurring changes in rat liver regarded as hepatic markers of peroxisome proliferators (PPs) [1].

Gene context of Fluazifop

• 2. Urinary excretion rate of the principal metabolite fluazifop, following dosing with the 5% formulation, was described by a two-compartment pharmacokinetic model; the average elimination half-lives of initial and terminal phases were 18 h and approximately 70 h, respectively [4].

Analytical, diagnostic and therapeutic context of Fluazifop

• Separation of the enantiomers of fluazifop and other 2-phenoxypropionic acids using chiral metal chelate additives in reversed-phase high-performance liquid chromatography [6].

References