Abstract
In recent decades, an increasing incidence of male infertility has been reported. Interestingly, and considering that pesticides have been used for a long time, the high incidence of this pathological state is concomitant with the increasing use of these chemicals, suggesting they are contributors for the development of human infertility. Data from literature highlight the ability of certain pesticides and/or their metabolites to persist in the environment for long periods of time, as well as to bioaccumulate in the food chain, thus contributing for their chronic exposure. Furthermore, pesticides can act as endocrine disrupting chemicals (EDCs), interfering with the normal function of natural hormones (which are responsible for the regulation of the reproductive system), or even as obesogens, promoting obesity and associated comorbidities, like infertility. Several in vitro and in vivo studies have focused on the effects and possible mechanisms of action of these pesticides on the male reproductive system that cause sundry negative effects, even though through diverse mechanisms, but all may lead to infertility. In this review, we present an up-to-date overview and discussion of the effects, and the metabolic and molecular features of pesticides on somatic cells and germinal tissues that affect germ cell differentiation.
Highlights
Infertility is a global public health problem, involving developed and developing countries [1]
Even though there are no reliable numbers for the global prevalence of infertility, recent studies have reported that infertility rates, which ranged from 7–8% in the 1960s, have increased drastically to current numbers of 20 to 35% [3]
We focus on the effects and mechanisms of action of pesticides with potential obesogenic action on the somatic testicular cells, testicular tissue, and metabolism that may result in male infertility
Summary
Infertility is a global public health problem, involving developed and developing countries [1]. As a matter of fact, since the 1970s, obesity has tripled [15], and, nowadays, is recognized that accumulation of toxic substances and lipid-soluble endocrine disruptors in fat tissue contributes to the amplification of the deleterious effects induced by increased body weight [16]. In line with this fact, storage of toxicants and obesogenic compounds in reproductive organs has been described, due to the high lipid content of these tissues, which may cause testicular dysgenesis syndrome, including atrophy of seminiferous tubules and germ cell degeneration [17]. Some methodologies used for the detection of pesticide and their metabolites, as well as metabolic pathway changes will be discussed
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