**3.3 Toxicity on female reproductive system**

Toxic effects of insecticides on female reproductive system were shown in different studies; and, it is concluded that insecticides disrupt female endocrine system and cause alterations in reproductive organs and germ cells [24]. Insecticides disrupt ovarian physiology. This is a two-way street as altering organ functions causes hormone secretion changes and this endocrine changes mostly affect the female reproductive system and result with dysfunctions via HPG axis. Disrupted hormone synthesis, altered follicular maturation, disrupted ovarian cycle, pregnancy time prolong, stillbirth and infertility are linked to oxidative imbalance in the cells, and eventually lead to DNA damage, inflammation and apoptosis induction [34].

It has been speculated that pesticides have important role in slaughtering buffaloes reproductive defects. This could be associated with follicle membrane permeability features that permit xenobiotics entrance to the system. Higher concentrations of insecticides including DDT, eldrine, endosulphan and butachlor were detected in ovary than serum. This could make a way for follicular wall alterations and more insecticide entrance to the cellular system. In addition, insecticides could affect germ cells at primordial phases resulting in infertility in adult stage [5].

In wild birds such as female bobwhite quail (*Colinus virginianus*), parathion exposure caused reduction of egg production, impairment of follicular cycle, and reduction of LH and progesterone levels. Organophosphate (methyl parathion/*phosphamidon/quinalphos) administration of white-throated munia (Lonchura malabarica) caused inhibition of two important enzymes: Δ5-3βhydroxysteroid dehydrogenase (3βHSD) and 17β-hydroxysteroid* dehydrogenase (17βHSD), playing key role in estrogen and progesterone production inhibition [32].

Endosulfan, an organochlorine, triggered apoptosis via oxidative stress induction in the follicle cells. Moreover, it induced the expressions of steroidogenic acute regulatory protein (StAR), CYP19A1a and aromatase, causing improper ovarian maturation. DDT exposure caused ovulation time alterations via inhibiting CYP450-side chain cleavage enzyme, progesterone receptor, estrogen sulfotransferase, cyclooxygenase-2 (COX-2) and epidermal growth factor (epiregulin) [34].

In female reproductive system, chlorpyrofos cause alterations in uterine weight and morphology via inducing surface epithelium and myometrium thickness [35]. In addition, chlorpyrofos could qualify as an ovotoxic and embryotoxic agent while mimicking estrogen and altering embryonic hatching, cell proliferation and apoptosis in zebrafish. Furthermore, chlorpyrifos reduces the levels of serum sex hormones such as LH, estrogen and progesterone [36, 37].

Toxic effects mechanisms of insecticides in female reproductive system are schematized in **Figure 2**.

#### **Figure 2.**

*Toxic effects mechanisms of insecticides in female reproductive system (FSH; follicle-stimulating hormone, LH; luteinizing hormone, ER; estrogen, ROS; reactive oxygen species, Cox2; Cyclooxygenase-2, StAr; Steroidogenic acute regulatory protein) [34].*

**243**

**Author details**

Mehtap Kara\* and Ezgi Öztaş

University, Istanbul, Turkey

provided the original work is properly cited.

Faculty of Pharmacy, Department of Pharmaceutical Toxicology, Istanbul

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

\*Address all correspondence to: mehtap.kara@istanbul.edu.tr

*Reproductive Toxicity of Insecticides*

mechanisms of the insecticides.

The authors declare no conflict of interest.

**Conflict of interest**

**4. Conclusions**

*DOI: http://dx.doi.org/10.5772/intechopen.92890*

Due to fact that insecticides may affect directly either male or female reproductive system as well as alter endocrine balance, eliminating or reducing the usage of insecticides is still a major concern. Considering literature data, many of insecticides caused infertility or developmental abnormalities by several pathways, and it is urgent to create awareness. Since, a huge amount of the data was obtained based on the rodent studies, further studies are needed to enlighten the toxic effects of insecticides on livestock. Furthermore, it would be possible to develop more effective and reduced-cost of stockbreeding by the clarification of possible molecular
