Repeated administration of fenitrothion alters renal functions via oxidative stress mechanism without inhibiting acetylcholinesterase activity in rats
Background: The main mechanism of fenitrothion (FNT) toxicity is by inhibiting the acetylcholinesterase enzyme, though studies have shown that FNT might also develop other toxicological manifestations, including oxidative stress. However, the kidney functions as well as oxidative stress status after...
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Biome Scientia
2020-11-01
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Series: | Life Sciences, Medicine and Biomedicine |
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Online Access: | http://biomescientia.com/index.php/lsmb/article/view/70 |
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author | Nur Afizah Yusoff Izzah Irdina Juremi Siti Balkis Budin Izatus Shima Taib |
author_facet | Nur Afizah Yusoff Izzah Irdina Juremi Siti Balkis Budin Izatus Shima Taib |
author_sort | Nur Afizah Yusoff |
collection | DOAJ |
description | Background: The main mechanism of fenitrothion (FNT) toxicity is by inhibiting the acetylcholinesterase enzyme, though studies have shown that FNT might also develop other toxicological manifestations, including oxidative stress. However, the kidney functions as well as oxidative stress status after repeated exposure to FNT is not well documented. Objective: The present study was conducted to evaluate the kidney functions and oxidative stress status after exposure to low doses of FNT. Materials and Methods: 24 male Sprague-Dawley rats were divided randomly into three groups (n = 8/group): control, which received 1 mg/ml corn oil; FNT 10, which received 10 mg/kg (BW) FNT; and FNT20 which received 20 mg/kg (BW) FNT. The corn oil and FNT were fed orally for 28 consecutive days. At the end of the study, the blood was taken, and the kidney was obtained for biochemistry evaluation and histological observation. Results: The AChE activity was significantly inhibited in the FNT20 group (p≤0.05) compared to the control group and FNT10 and the rats exhibited the signs and symptoms of toxicity such as lacrimation, piloerection, hypoactivity, and tremor. Plasma creatinine and BUN levels showed a significant increase (p≤0.05) in FNT treated groups, but the superoxide dismutase and glutathione level were significantly reduced (p≤0.05). The malondialdehyde and protein carbonyl level were elevated significantly (p≤0.05) in FNT treated groups. Histopathological observation revealed morphological changes, including atrophy of the glomerulus and presence of non-amyloid substances in FNT treated groups. Conclusion: Even at the dose that did not inhibit the AChE activity, FNT was found to reduce the renal function and induce oxidative damage on the kidney of male Sprague Dawley rats. |
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spelling | doaj.art-351575b8ddbb4bcab4058fef5cf623462022-12-21T22:05:14ZengBiome ScientiaLife Sciences, Medicine and Biomedicine2600-72072020-11-014910.28916/lsmb.4.9.2020.7048Repeated administration of fenitrothion alters renal functions via oxidative stress mechanism without inhibiting acetylcholinesterase activity in ratsNur Afizah Yusoff0Izzah Irdina Juremi1Siti Balkis Budin2Izatus Shima Taib3Programme of Biomedical Sciences, Centre of Diagnostic, Therapeutic and Investigations, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, 50300 Kuala Lumpur, MalaysiaProgramme of Biomedical Sciences, Centre of Diagnostic, Therapeutic and Investigations, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, 50300 Kuala Lumpur, Malaysia.Programme of Biomedical Sciences, Centre of Diagnostic, Therapeutic and Investigations, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, 50300 Kuala Lumpur, MalaysiaProgramme of Biomedical Sciences, Centre of Diagnostic, Therapeutic and Investigations, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, 50300 Kuala Lumpur, MalaysiaBackground: The main mechanism of fenitrothion (FNT) toxicity is by inhibiting the acetylcholinesterase enzyme, though studies have shown that FNT might also develop other toxicological manifestations, including oxidative stress. However, the kidney functions as well as oxidative stress status after repeated exposure to FNT is not well documented. Objective: The present study was conducted to evaluate the kidney functions and oxidative stress status after exposure to low doses of FNT. Materials and Methods: 24 male Sprague-Dawley rats were divided randomly into three groups (n = 8/group): control, which received 1 mg/ml corn oil; FNT 10, which received 10 mg/kg (BW) FNT; and FNT20 which received 20 mg/kg (BW) FNT. The corn oil and FNT were fed orally for 28 consecutive days. At the end of the study, the blood was taken, and the kidney was obtained for biochemistry evaluation and histological observation. Results: The AChE activity was significantly inhibited in the FNT20 group (p≤0.05) compared to the control group and FNT10 and the rats exhibited the signs and symptoms of toxicity such as lacrimation, piloerection, hypoactivity, and tremor. Plasma creatinine and BUN levels showed a significant increase (p≤0.05) in FNT treated groups, but the superoxide dismutase and glutathione level were significantly reduced (p≤0.05). The malondialdehyde and protein carbonyl level were elevated significantly (p≤0.05) in FNT treated groups. Histopathological observation revealed morphological changes, including atrophy of the glomerulus and presence of non-amyloid substances in FNT treated groups. Conclusion: Even at the dose that did not inhibit the AChE activity, FNT was found to reduce the renal function and induce oxidative damage on the kidney of male Sprague Dawley rats.http://biomescientia.com/index.php/lsmb/article/view/70antioxidantnon-amyloidoxidative stressorganophosphateoxidative damage |
spellingShingle | Nur Afizah Yusoff Izzah Irdina Juremi Siti Balkis Budin Izatus Shima Taib Repeated administration of fenitrothion alters renal functions via oxidative stress mechanism without inhibiting acetylcholinesterase activity in rats Life Sciences, Medicine and Biomedicine antioxidant non-amyloid oxidative stress organophosphate oxidative damage |
title | Repeated administration of fenitrothion alters renal functions via oxidative stress mechanism without inhibiting acetylcholinesterase activity in rats |
title_full | Repeated administration of fenitrothion alters renal functions via oxidative stress mechanism without inhibiting acetylcholinesterase activity in rats |
title_fullStr | Repeated administration of fenitrothion alters renal functions via oxidative stress mechanism without inhibiting acetylcholinesterase activity in rats |
title_full_unstemmed | Repeated administration of fenitrothion alters renal functions via oxidative stress mechanism without inhibiting acetylcholinesterase activity in rats |
title_short | Repeated administration of fenitrothion alters renal functions via oxidative stress mechanism without inhibiting acetylcholinesterase activity in rats |
title_sort | repeated administration of fenitrothion alters renal functions via oxidative stress mechanism without inhibiting acetylcholinesterase activity in rats |
topic | antioxidant non-amyloid oxidative stress organophosphate oxidative damage |
url | http://biomescientia.com/index.php/lsmb/article/view/70 |
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