Dioxin’s impact on sperm counts & Statement of Robert Moore from Our Stolen Future | The Silent War

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Dioxin’s impact on sperm counts & Statement of Robert Moore from Our Stolen Future

June 5, 2010 by Chemista

Posted in Dioxin, Endocrine Disruption, Methoxychlor, Our Stolen Future, Vinclozolin (Fungicide) | 2 Comments

2 Responses

on May 25, 2013 at 3:11 pm | Reply Chemista

wp admin took issue with this post as well as all the posts I’ve put up regarding sperm count deduction.

The following excerpt is from page 120 – 121 of Our Stolen Future.

Scientists understand less about dioxin than they do about the more straightforward hormone mimics or blockers, such as methoxychlor and vinclozolin, which cause disruption by binding with estrogen or androgen receptors. For this reason, Gray explains, he would be less confident predicting what might happen to humans based on animal experiments. Recent discoveries are, however, giving scientists increasing confidence that the responses in humans and animals are likely to be roughly similar. Researchers have found that dioxin acts almost exclusively through a receptor–one of the “orphan” receptors whose normal chemical messenger remains unknown. Although this receptor was first identified in animals, studies have shown that humans also have a fully functional aryl hydrocarbon, or Ah, receptor that binds with dioxin. Once dioxin occupies the receptor in a human cell, researchers have found that it binds to DNA in the cell nucleus, prompting many of the same changes in gene expression seen in animal experiments. Humans seem no less sensitive to this effect. But what happens afterward to produce all of dioxin’s disparate biological effects, including developmental disruption, remains a mystery.

However it happens, dioxin acts like a powerful and persistent hormone that is capable of producing lasting effects at very low doses–doses similar to levels found in the human population.

The outstanding irony is that the rats in Moore’s experiments passed the standard fertility tests with flying colors–tests typically used by the chemical industry to screen chemicals for safety. Almost all were able to impregnate females and produce the normal number of pups. The reason, Moore explains, is that the rats are incredibly robust breeders, producing ten times more sperm than they really need to reproduce. Tests have found that a toxic chemical can knock out 99% of a rat’s sperm and still have no effect on his ability to reproduce.

Humans, by comparison, are inefficient breeders, who tend to produce barely the number of sperm required for successful fertilization. Moore describes the human male sperm count as “borderline pathological” for many individuals even without the assault of endocrine-disrupting chemicals. If Moore is correct and if long-term declines in human sperm count continue, our species faces a troubling prospect. Such a drop could have a devastating impact on human fertility.

In utero and lactational exposure of male rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin *1: 3. Effects on spermatogenesis and reproductive capability

Thomas A. Mably*, 2, Donald L. Bjerke*, Robert W. Moore†, *, Annette Gendron-Fitzpatrick‡ and Richard E. Peterson.
* School of Pharmacy, University of Wisconsin, Madison, Wisconsin 53706, USA
† Environmental Toxicology Center, University of Wisconsin, Madison, Wisconsin 53706, USA
‡ Research Animal Resource Center, University of Wisconsin, Madison, Wisconsin 53706, USA
Received 16 September 1991; accepted 7 February 1992. Available online 24 September 2004.

Abstract

When administered in overtly toxic doses to postweanling male rats, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produces adverse effects on the reproductive system including a decrease in spermatogenesis. Because the male reproductive system may be particularly susceptible to toxic insult during the perinatal period, the effects of in utero and lactational TCDD exposure on its development were examined. Male rats born to dams given TCDD (0.064, 0.16, 0.40, or 1.0 μg/kg, po) or vehicle on Day 15 of gestation were evaluated at various stages of development; effects on spermatogenesis and male reproductive capability are reported herein. Testis, epididymis, and cauda epididymis weights were decreased in a dose-related fashion at 32, 49, 63, and 120 days of age, that is, when males were at the juvenile, pubertal, postpubertal, and mature stages of sexual development, respectively. When measured on Days 49, 63, and 120, daily sperm production by the testis was reduced at the highest maternal TCDD dose to 57–74% of the control rate. Cauda epididymal sperm reserves in 63- and 120-day-old males were decreased to as low as 25 and 44%, respectively, of control values, although the motility and morphology of these sperm appeared to be unaffected. The magnitude of the effects described above tended to lessen with time; nevertheless, the decreases in epididymis and cauda epididymis weights, daily sperm production, and cauda epididymal sperm number were statistically significant at the lowest maternal dose tested (0.064 μg TCDD/kg) on Day 120 and at most earlier times. To determine if in utero and lactational TCDD exposure also affects male reproductive capability, rats were mated at approximately 70 and 120 days of age with control females. Little if any effect on fertility was seen, and the survival and growth of offspring was unaffected. These results are not inconsistent with the pronounced reductions in daily sperm production and cauda epididymal sperm reserves caused by perinatal TCDD exposure since rats produce and ejaculate far more sperm than are required for normal fertility. The TCDD-induced reduction in spermatogenesis cannot be accounted for by concurrent effects on plasma follicle-stimulating hormone or androgen concentrations or by undernutrition. To investigate the nature of the spermatogenic lesion, leptotene spermatocyte to Sertoli cell ratios were determined. The finding that in utero and lactational TCDD exposure did not affect these ratios in 49-, 63-, and 120-day-old rats suggests that the decrease in spermatogenesis is caused by impaired division and/or increased attrition of cells during the conversion of leptotene spermatocytes to spermatozoa and/or by a reduction in Sertoli cell number. Regardless of mechanism, results from this study show that spermatogenesis is much more susceptible to TCDD when exposure occurs perinatally than when it follows weaning. The reduction in spermatogenesis occurs at doses of TCDD that are among the lowest reported to cause toxicity in the rat.
on May 27, 2013 at 2:38 am | Reply Testosterone

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