Abstract
S-metolachlor is a chloroacetanilide herbicide widely used in the agriculture to control weeds and was demonstrated that it increases the activity of the aromatase enzyme in cell cultures, which may culminate as endocrine disruption action in vivo. To investigate this hypothesis, prepubertal Wistar male rats were exposed to metolachlor (5 or 50 mg/kg/day, NOEL for reproductive toxicity: 23.5–26.0 mg/kg/day) from PND23 (postnatal day) to PND53. During this period, the growth of the animals and the age and weight at puberty were recorded. In PND53, tissues were collected and the analysis of LH, FSH, testosterone, dihydrotestosterone (DHT), estradiol serum concentrations, morphometric evaluation of the seminiferous epithelium, and weight of the testes and the seminal vesicle (undrained and drained) was performed (Statistical difference: P < 0.05). Metolachlor caused an increase in serum concentrations of testosterone, estradiol, and FSH and a reduction in DHT but did not alter the LH. There were also observed a higher amount of fluid in the seminal vesicles, precocious puberty, and changes in morphology of the seminiferous epithelium of treated animals. We demonstrated in this paper that prepubertal exposure to S-metolachlor caused changes in reproductive endocrinology of male rats.
Highlights
The endocrine system may be the main target for the toxic manifestation of pesticides and may result in reproductive alterations, especially in steroid-hormone-dependent functions [1, 2]
The effect of daily exposure to the herbicide on the reproductive endocrinology was assessed by determining the serum concentrations of testosterone, estradiol, DHT, LH, and FSH in blood samples from 53-day-old rats
The focus of this study was to verify the toxicological effects on the reproductive parameters of a commercial formulation of metolachlor in vivo, using prepubertal male rats as an experimental model
Summary
The endocrine system may be the main target for the toxic manifestation of pesticides and may result in reproductive alterations, especially in steroid-hormone-dependent functions [1, 2]. Endocrine disruptors were defined by Kavlock et al [3] as exogenous agents that interfere with the production, release, transport, metabolism, binding, action, or elimination of natural hormones responsible for the maintenance of homeostasis and the regulation of developmental processes. These disturbances may potentially cause risk to population by impairing their capacity to reproduce [4], being that occupational exposure to pesticides has been linked to a reduction in the quality of semen and a greater rate of infertility and miscarriage [5, 6]. Compared to metolachlor (50% S-enantiomer and 50% R-enantiomer), S-metolachlor represents an important reduction in risk to users, consumers, and the environment [7, 8] since formulations of S-metolachlor in proportions above 80% have higher herbicide activity and a smaller amount of product may be used [9]
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