In vitro hepatotoxicity of alachlor and its by-products
Copyright 2002 John Wiley & Sons, Ltd..
During water treatment, potentially hazardous chemical by-products may be formed. Alachlor (2-chloro-N-(2, 6-diethylphenyl)-N-(methoxymethyl) acetamide) is a widely used pre-emergence herbicide. The present study investigated the toxicity of alachlor and its disinfection by-products on freshly isolated rat hepatocytes. Hepatocytes were harvested by a collagenase perfusion technique and were exposed to different concentrations of alachlor and its by-products for up to 2 h. Cell viability, the leakage of aspartate transaminase (AST) and alanine transaminase (ALT) and glutathione (GSH) depletion were determined throughout the incubation period. The cell viability of the hepatocytes exposed to 100 microg ml(-1) alachlor was decreased by 20% compared with the control after 60 min of incubation. At the same concentration of alachlor the leakage of ALT and AST was increased by 56% and 45%, respectively. Cell viability of the hepatocytes was decreased upon exposure to 2-chloro-N-(3-chloro-2,6-diethylphenyl)-N-(methoxymethyl) acetamide (CCDMA) and 2-chloro-N-(3-chloro-2,6-diethylphenyl) acetamide (CCDA)--the by-products of alachlor and chlorine--after 60 min of exposure. At 100 microg ml(-1) CCDMA the AST leakage was increased significantly (73%) after 30 min of incubation. The reaction mixture of alachlor (100 microg ml(-1)) and chlorine dioxide (1 ppm) caused significant increases in cell loss and ALT and AST levels by 22%, 40% and 34%, respectively, as early as 15 min incubation. Alachlor (100 and 200 microg ml(-1)) caused significant decreases in GSH contents (62%) in isolated hepatocytes. The reaction mixture of alachlor and chlorine dioxide led to significant glutathione depletion (44%) after 60 min of incubation. The by-products of alachlor and chlorine--CCDMA and CCDA--depleted GSH almost completely (93%). This investigation suggested that the by-products formed from the reaction of alachlor and chlorine decreased GSH and increased the leakage of liver enzymes, especially AST.
Medienart: |
Artikel |
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Erscheinungsjahr: |
2002 |
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Erschienen: |
2002 |
Enthalten in: |
Zur Gesamtaufnahme - volume:22 |
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Enthalten in: |
Journal of applied toxicology : JAT - 22(2002), 1 vom: 22. Jan., Seite 31-5 |
Sprache: |
Englisch |
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Beteiligte Personen: |
El-Sakka, Sahar [VerfasserIn] |
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Anmerkungen: |
Date Completed 30.04.2002 Date Revised 22.09.2019 published: Print Citation Status MEDLINE |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM116960590 |
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100 | 1 | |a El-Sakka, Sahar |e verfasserin |4 aut | |
245 | 1 | 0 | |a In vitro hepatotoxicity of alachlor and its by-products |
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520 | |a Copyright 2002 John Wiley & Sons, Ltd. | ||
520 | |a During water treatment, potentially hazardous chemical by-products may be formed. Alachlor (2-chloro-N-(2, 6-diethylphenyl)-N-(methoxymethyl) acetamide) is a widely used pre-emergence herbicide. The present study investigated the toxicity of alachlor and its disinfection by-products on freshly isolated rat hepatocytes. Hepatocytes were harvested by a collagenase perfusion technique and were exposed to different concentrations of alachlor and its by-products for up to 2 h. Cell viability, the leakage of aspartate transaminase (AST) and alanine transaminase (ALT) and glutathione (GSH) depletion were determined throughout the incubation period. The cell viability of the hepatocytes exposed to 100 microg ml(-1) alachlor was decreased by 20% compared with the control after 60 min of incubation. At the same concentration of alachlor the leakage of ALT and AST was increased by 56% and 45%, respectively. Cell viability of the hepatocytes was decreased upon exposure to 2-chloro-N-(3-chloro-2,6-diethylphenyl)-N-(methoxymethyl) acetamide (CCDMA) and 2-chloro-N-(3-chloro-2,6-diethylphenyl) acetamide (CCDA)--the by-products of alachlor and chlorine--after 60 min of exposure. At 100 microg ml(-1) CCDMA the AST leakage was increased significantly (73%) after 30 min of incubation. The reaction mixture of alachlor (100 microg ml(-1)) and chlorine dioxide (1 ppm) caused significant increases in cell loss and ALT and AST levels by 22%, 40% and 34%, respectively, as early as 15 min incubation. Alachlor (100 and 200 microg ml(-1)) caused significant decreases in GSH contents (62%) in isolated hepatocytes. The reaction mixture of alachlor and chlorine dioxide led to significant glutathione depletion (44%) after 60 min of incubation. The by-products of alachlor and chlorine--CCDMA and CCDA--depleted GSH almost completely (93%). This investigation suggested that the by-products formed from the reaction of alachlor and chlorine decreased GSH and increased the leakage of liver enzymes, especially AST | ||
650 | 4 | |a Journal Article | |
650 | 7 | |a Acetamides |2 NLM | |
650 | 7 | |a Disinfectants |2 NLM | |
650 | 7 | |a Herbicides |2 NLM | |
650 | 7 | |a Water Pollutants, Chemical |2 NLM | |
650 | 7 | |a alachlor |2 NLM | |
650 | 7 | |a 24S2S61PXL |2 NLM | |
650 | 7 | |a Chlorine |2 NLM | |
650 | 7 | |a 4R7X1O2820 |2 NLM | |
650 | 7 | |a Aspartate Aminotransferases |2 NLM | |
650 | 7 | |a EC 2.6.1.1 |2 NLM | |
650 | 7 | |a Alanine Transaminase |2 NLM | |
650 | 7 | |a EC 2.6.1.2 |2 NLM | |
650 | 7 | |a Glutathione |2 NLM | |
650 | 7 | |a GAN16C9B8O |2 NLM | |
700 | 1 | |a Salem, Ezz El-Din M |e verfasserin |4 aut | |
700 | 1 | |a Abdel-Rahman, Mohamed S |e verfasserin |4 aut | |
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