**4. Conclusions**

*Animal Reproduction in Veterinary Medicine*

apoptosis induction [34].

adult stage [5].

schematized in **Figure 2**.

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

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

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

Toxic effects mechanisms of insecticides in female reproductive system are

*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* 

hormones such as LH, estrogen and progesterone [36, 37].

**242**

**Figure 2.**

*acute regulatory protein) [34].*

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 mechanisms of the insecticides.
