Influence of subacute treatment of some plant growth regulators on serum marker enzymes and erythrocyte and tissue antioxidant defense and lipid peroxidation in rats

Abstract

This study aims to investigate the effects of the plant growth regulators (PGRs) (2,3,5-triiodobenzoic acid (TIBA), Naphthaleneacetic acid (NAA), and 2,4-dichlorofenoxyacetic acid (2,4-D)) on serum marker enzymes (aspartate aminotransferase (AST), alanin aminotransferase (ALT), creatine phosphokinase (CPK), and lactate dehydrogenase (LDH)), antioxidant defense systems (reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase (GST), and catalase (CAT)), and lipid peroxidation content (malondialdehyde = MDA) in various tissues of rats. 50 and 100 ppm of PGRs as drinking water were administered orally to rats (Sprague-Dawley albino) ad libitum for 25 days continuously. The PGRs treatment caused different effects on the serum marker enzymes, antioxidant defense systems, and the MDA content in experimented rats compared to controls. Results showed that TIBA caused a significant decrease in serum AST activity with both the dosage whereas serum CPK was significantly increased with 100 ppm dosage of TIBA. Meanwhile, serum AST, CPK, and LDH activities were significantly increased with both dosage of NAA and 2,4-D. The lipid peroxidation end-product MDA significantly increased in the all tissues treated with both dosages of PGRs without any change in the brain and erythrocyte of rats treated with both the dosages of 2,4-D. The GSH depletion in the kidney and brain tissues of rats treated with both dosages of PGRs was found to be significant. Furthermore, the GSH depletion in the erythrocyte of rats treated with both dosages of PGRs except 50 ppm dosage of 2,4-D was significant too. Also, the GSH level in the liver was significantly depleted with 50 ppm of 2,4-D and NAA, whereas the GSH depletion in the same tissue did not significantly change with the treatment. The activity of antioxidant enzymes was also seriously affected by PGRs; SOD significantly decreased in the liver, heart, kidney, and brain of rats treated with both dosages of NAA, whereas the SOD activity in the erythrocytes, liver, and heart was either significantly decreased or not changed with two doses of 2,4-D and TIBA. Although the CAT activity significantly increased in the erythrocyte and brain of rats treated with both doses of PGRs, it was not changed in the liver, heart, and kidney. Meanwhile, the ancillary enzyme GR activity significantly increased in the brain, heart, and liver but decreased in the erythrocyte and kidney of rats treated with both doses of PGRs. The drug-metabolizing enzyme GST activity significantly increased in the heart and kidney but decreased in the brain and erythrocytes of rats treated with both dosages of PGRs. As a conclusion, the results indicate that PGRs might affect antioxidant potential enzymes, the activity of hepatic damage enzymes, and lipid peroxidation dose independently. Also, the rats resisted to oxidative stress via antioxidant mechanism but the antioxidant mechanism could not prevent the increases in lipid peroxidation in rat's tissues. These data, along with t...

A comparison of the effects of 1,4-naphthoquinone and 2-hydroxy-1,4-naphthoquinone (lawsone) on indole-3-acetic acid (IAA)-induced growth of maize coleoptile cells

“…The results presented here also showed that in the presence of IAA, both naphthoquinones at 1000 µM induced a 30% lower increase in HCF III reduction by the maize coleoptile segments compared to variant without auxin. In trying to explain this finding, we assumed that auxin, which is able to change the fluidity of the lipid systems and weaken the interactions between their components (De Melo et al 2004;Celik et al 2006) may disturb the integration of naphthoquinones into the plasma membrane (hypothesis proposed by Lüthje et al 1992) and subsequently decrease HCF III reduction. It should also be added that IAA alone stimulated HCF III reduction as was previously shown by Lekacz and Karcz (2006).…”

Oxidative Stress Induced by the 2,4-Dichlorophenoxyacetic Herbicide

“…In vitro reports have looked, especially, at the effects of 2,4-D on hepatocytes and red blood cells (Palmeira et al, 1995;Bukowska, 2003). In vivo oxidative activity has been studied in many species including yeast, plants, fish and rats (Romero-Puerats et al, 2004;Teixeira et al, 2004;Oruc and Uner, 1999;Celik et al, 2006). Lipid peroxidation has been suggested as one of the molecular mechanisms involved in pesticide-induced toxicity; as a consequence such pesticides can disturb the biochemical and physiological functions of some organs.…”

“…The first important study was done by Celik et al (2006), who studied the effects of 2,4-D on serum marker enzymes, erythrocyte and tissue antioxidant defense and lipid peroxidation in rats. The authors found that the administration of 1.5 and 3mg/day of 2,4-D during 25 days induced in vivo oxidation.…”

Photocatalytic Degradation of 2, 4-D and Transition of Endocrine Disruptive Activity Using Transcriptome Based Bioassay in Zebrafish Embryos

“…Its toxicity on non-target organisms has been a topic of extensive research, with some studies suggesting that 2, 4-D can induce oxidative damage to animal tissues [10]- [15] and the measurements of antioxidative enzyme activities like glutathione peroxidase in fish have been used to assess the oxidative damage [16]. Currently, various biomarkers have been used to impartially measure endocrine disruptive potency and understand the underlying mechanisms [17].…”