**6. Female endocrine disruption**

Arsenic is well recognized for its reproductive toxicity, as in case of male reproductive system it is accounted that to hinder activities of spermatogenetic enzymes and impede spermatogenesis [28]. Arsenic may act on brain or pituitary or and on germ line cells and affect the female reproductive system such as it reduce ovarian steroidogenesis, prolong diestrus, degenerate ovarian follicles and decrease the plasma level of estradiol and progesterone [46]. Furthermore reduced plasma gonadotrophin level may decline activities of ovarian 3β- HSD (Hydroxysteroid dehydrogenase) and 17β- HSD (Hydroxysteroid dehydrogenase), which are essential regulatory enzymes for steroidogenesis [47]. As it is observed that low plasma level of estradiol may be the cause of diestrus. Furthermore, arsenic exposure in human causes reproductive toxicity, including elevated incidence of miscarriages, still birth and low birth weight in offspring [17]. Similarly, it also effect on viability in the conceptus, dam mortality and weight gain of fetus [48]. Arsenic plays a potential role in disruption of female hormonal function, such as interfering hormone synthesis and hormone normal function. All hormones are differing in their structure and function and have various routes of synthesis with numerous steps. Arsenic exposure through pesticides and other products may disrupt the chain of hormone synthesis such as inhibition of estrogen biosynthesis [49], by preventing the conversion of androgen into estrogen [50]. Methylated arsenic may interfere in dopamine beta hydroxylase activity resulting in reduced conversion of dopamine into nor-epinephrine [19] which may lead to hindrance of hypothalamic catecholamine activity involved in generation of pro-estrus surge in LH, which stimulates ovulation [51]. It also inhibits various other enzymes which are involved in progesterone synthesis [52]. Disruption in LH timing surge could alter the viability and quality of oocytes [51] and inhibition of progesterone secretion may lead to poor conception (**Figure 1**) [48]. The distorted estrogen signaling may cause over expression of estrogen receptors through promoter region hypo-methylation and cause epigenetic change to produce estrogen like effect by direct or indirect stimulation of estrogen receptors.
