A glyphosate-based herbicide induces necrosis and apoptosis in mature rat testicular cells in vitro, and testosterone decrease at lower levels

被引:159
作者
Clair, Emilie [1 ,2 ,3 ]
Mesnage, Robin [1 ,2 ,3 ]
Travert, Carine [1 ]
Seralini, Gilles-Eric [1 ,2 ,3 ]
机构
[1] Univ Caen Basse Normandie, EA2608, Inst Biol, F-14032 Caen, France
[2] Univ Caen Basse Normandie, Risk Pole MRSH CNRS, F-75008 Paris, France
[3] Univ Caen Basse Normandie, CRIIGEN, F-75008 Paris, France
关键词
Roundup; Glyphosate; Testicular cells; Cytotoxicity; Endocrine disruption; DYSGENESIS SYNDROME; ENDOCRINE DISRUPTORS; LEYDIG-CELLS; ROUNDUP; STEROIDOGENESIS; TOXIN; DEATH; SEMEN; FORMULATION; INHIBITION;
D O I
10.1016/j.tiv.2011.12.009
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
The major herbicide used worldwide, Roundup, is a glyphosate-based pesticide with adjuvants. Glyphosate, its active ingredient in plants and its main metabolite (AMPA) are among the first contaminants of surface waters. Roundup is being used increasingly in particular on genetically modified plants grown for food and feed that contain its residues. Here we tested glyphosate and its formulation on mature rat fresh testicular cells from 1 to 10000 ppm, thus from the range in some human urine and in environment to agricultural levels. We show that from 1 to 48 h of Roundup exposure Leydig cells are damaged. Within 24-48 h this formulation is also toxic on the other cells, mainly by necrosis, by contrast to glyphosate alone which is essentially toxic on Sertoli cells. Later, it also induces apoptosis at higher doses in germ cells and in Sertoli/germ cells co-cultures. At lower non toxic concentrations of Roundup and glyphosate (1 ppm), the main endocrine disruption is a testosterone decrease by 35%. The pesticide has thus an endocrine impact at very low environmental doses, but only a high contamination appears to provoke an acute rat testicular toxicity. This does not anticipate the chronic toxicity which is insufficiently tested, and only with glyphosate in regulatory tests. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:269 / 279
页数:11
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