Consumption of soy isoflavones during the prepubertal phase delays puberty and causes hypergonadotropic hypogonadism with disruption of hypothalamic-pituitary gonadotropins regulation in male rats

Toxicological Effects of Naturally Occurring Endocrine Disruptors on Various Human Health Targets: A Rapid Review

“…The main route of exposure to N-EDCs was through the diet, which accounted for 59% of cases. This is supported by both human studies (observational and epidemiological data) and in vivo models, which included ad libitum oral administration and gavage [ 22 , 27 ]. Among the papers in which diet was the source of exposure to N-EDCs, the records focused on soy, and the isoflavones of soy products were the most prevalent source (86.4%), followed by stilbenes (4.5%), coffee (4.5%), phytosterol (2.3%) and mesquite (2.3%).…”

“…Flavonoids act directly on the 3β-hydroxysteroid dehydrogenase (HSD) enzyme, while the mycotoxin aflatoxin B1 can also affect cytochrome P450 enzymes, thereby inhibiting Leydig cell activity and causing testosterone deficiency. The intake of flavonoids [ 18 , 22 , 28 , 29 , 35 , 39 ], zearalenone [ 56 ] and microcystin [ 60 ] has been correlated with a decrease in serum testosterone levels, although Messina et al and Lephardt et al reported from clinical trials that this correlation was not statistically significant [ 6 , 52 ].…”

“…In the same study, resveratrol disrupted the HPG axis and altered the weight of testes and the brain in male offspring. N-EDCs, such as PEs or phytosterols, have been seen to compromise the HPG axis [ 22 , 28 , 63 ]. Oliveira and colleagues observed that prepubertal consumption of soy isoflavone altered the mRNA expression levels of genes regulating the HPT (hypothalamus–pituitary gland–testis) axis, causing hypergonadotropic hypogonadism [ 22 ].…”

“…N-EDCs, such as PEs or phytosterols, have been seen to compromise the HPG axis [ 22 , 28 , 63 ]. Oliveira and colleagues observed that prepubertal consumption of soy isoflavone altered the mRNA expression levels of genes regulating the HPT (hypothalamus–pituitary gland–testis) axis, causing hypergonadotropic hypogonadism [ 22 ]. Jing S. et al reported similar detrimental effects on the HPG axis, such as changes in gene expression and steroid hormone secretion in rats exposed to zearalenone.…”

“…The therapeutic use of many N-EDCs, combined with their toxicological effects (duplex effects), often results in controversial and confusing information. Few clinical or epidemiological results are available from humans, while a slightly higher number of toxicological findings are based on in vitro studies [ 8 , 19 , 20 , 21 ] and rodent [ 15 , 22 , 23 ] models. It is important to note that a substance may be an EDC for one species and not for another [ 16 ].…”