Enantioselective Damage of Diclofop Acid Mediated by Oxidative Stress and Acetyl-CoA Carboxylase in Nontarget Plant Arabidopsis thaliana

2012 ◽  
Vol 46 (15) ◽  
pp. 8405-8412 ◽  
Author(s):  
Qiong Zhang ◽  
Meirong Zhao ◽  
Haifeng Qian ◽  
Tao Lu ◽  
Quan Zhang ◽  
...  
Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 953
Author(s):  
Vitor Teixeira ◽  
Ibrahim Mohamed ◽  
Jean-Claude Lavoie

Premature neonates are submitted to an early-life oxidative stress from parenteral nutrition, which is vitamin C (VC) deficient and induces low endogenous levels of glutathione. The oxidative stress caused by these deficiencies may permanently affect liver glycolysis and lipogenesis. This study evaluates the short- and long-term effects of neonatal VC and cysteine deficient diets on redox and energy metabolism. Three-day-old Hartley guinea pigs from both sexes were given a regular or a deficient diet (VC, cysteine, or both) until week 1 of life. Half of the animals were sacrificed at this age, while the other half ate a complete diet until 12 weeks. Liver glutathione and the activity and protein levels of glucokinase, phosphofructokinase, and acetyl-CoA-carboxylase were measured. Statistics: factorial ANOVA (5% threshold). At 1 week, all deficient diets decreased glutathione and the protein levels of glucokinase and phosphofructokinase, while cysteine deficiency decreased acetyl-CoA-carboxylase levels. A similar enzyme level was observed in control animals at 12 weeks. At this age, VC deficiency decreased glutathione, while cysteine increased it. Acetyl-CoA-carboxylase protein levels were increased, which decreased its specific activity. Early-life VC and cysteine deficiencies induce neonatal oxidative stress and an adult-like metabolism, while predisposing to increased lipogenic rates during adulthood.


2020 ◽  
Vol 27 (24) ◽  
pp. 30118-30132 ◽  
Author(s):  
Mohammad H. Abukhalil ◽  
Omnia E. Hussein ◽  
May Bin-Jumah ◽  
Sultan A. M. Saghir ◽  
Mousa O. Germoush ◽  
...  

1995 ◽  
Vol 48 (12) ◽  
pp. 1907 ◽  
Author(s):  
SA Henderson ◽  
J Oconnor ◽  
AR Rendina ◽  
GP Savage ◽  
GW Simpson

(3aα,6β,6aα)-6-Methyltetrahydro-1H-thieno[3,4-b]pyrrol-2(3H)-one (2) was prepared as a crippled analogue of biotin. The key synthetic step involved hydrogenation of 6-methyl-1H- thieno [3,4-b]pyrrol-2(3H)-one on palladium to introduce the necessary all-cis configuration. Both compounds were weak inhibitors of the biotin-dependent wheat acetyl-CoA carboxylase compared to substrates or the potent herbicidal inhibitors of this enzyme, but were more potent than biotin or imidazolidone. Neither compound inhibited the biotin-dependent transcarboxylase component of bacterial acetyl-CoA carboxylase, nor did they significantly inhibit the growth of Arabidopsis thaliana.


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