Rodent reproduction

Rodent reproductive/developmental toxicity study (segment 2) 14... 

Wickramaratne GA, Foster JR, Ellis MK, and Tomenson JA (1998) Molinate Rodent reproductive toxicity and its relevance to humans - A review. Regulatory Toxicology and Pharmacology 27 112-118. 

Milligan, R.S. Pheromone and Rodent Reproductive Physiology. Symp. Zool. Soc. London 45, 251-275 (1980). 

Reproductive Effects. Phthalates have been shown to cause reproductive effects in rats and mice but primates are resistant to these effects. This may be due in part to pronounced differences in the way in which phthalates are metabolized by rodents and primates, including humans. 

The cytokine leptin is secreted by adipocytes (fat cells) in proportion to the size of the adipose dq>ot and circulates via the bloodstream to the brain, where it ultimately affects feeding behavior, endocrine systems including reproductive function and, at least in rodents, energy expenditure. The major effect of Lqrtin is on the hy-pothalamous, where it suppresses appetite and hence food intake. Leptin exerts its effects via binding to the leptin receptor in the brain (specifically in the hypothalamus), which activates the JAK-STAT Pathway. 

Apart from the wide range of neurotoxic and behavioral effects caused by OPs, many of which can be related to inhibition of AChE, other symptoms of toxicity have been reported. These include effects on the immune system of rodents (Galloway and Handy 2003), and effects on fish reproduction (Cook et al. 2005 Sebire et al. 2008). In these examples, the site of action of the chemicals is not identified. Indirect effects on the immune system or on reproduction following initial interaction with AChE of the nervous system cannot be ruled out. It is also possible that OPs act directly on the endocrine system or the reproductive system, and phosphorylate other targets in these locations (Galloway and Handy 2003). 

The accessory system in male and female rodents then, is susceptible to a variety of modulatory influences, which in turn affects the functions of the reproductive system. The interactions of hormones with transmitters at each stage along the AOS pathway (Fig. 5.9) form the... 

The consistency of the effects noted above and in Chap. 5 which modulate reproduction and involve the operation of the AOS, are unlikely to be wholly artifacts of captivity. Nevertheless, it needs to be shown which of the influences on male and female fertility have relevance to natural populations (Fig. 7.12). As mentioned, very few experiments on free-living social mammals have been reported, since the logistical problems of stimulus manipulation and control are formidable. A semi-feral population is an acceptable substitute, and provides some means of testing assumptions on the relevance of findings on caged laboratory-bred rodents. 

Marchlewska-Koj A. (1997). Sociogenic stress and reproductive activity in rodents. Neurosci Biobehav Rev 21, 699-703. 

Tricresyl phosphate (a complex mixture containing tri-o, Xn-m-, and tri-para-cresyl phosphate that is used in certain hydraulic fluids) and TOCP are demonstrated testicular toxicants in rodents (Carlton et al. 1987 Somkuti et al. 1987a, 1987b). Tricresyl phosphate also has been shown to impair in vivo fertility in rats and mice (Carlton et al. 1987 Chapin et al. 1988a). In addition, tricresyl phosphate-treated female rats displayed vacuolar cytoplasmic alteration of ovarian interstitial cells (Carlton et al. 1987 NTP 1994). Reproductive effects have also been seen after oral exposure to butylated triphenyl phosphate (Latendresse et al. 1994b). 

An organophosphate ester commonly used in hydraulic fluids, tricresyl phosphate (TCP), and tri-ortho-cresyl phosphate (TOCP), a possible contaminant of older formulations of TCP, have been shown to alter testicular morphology, testicular function, and reproductive function in rodents after oral exposure (Carlton et al. 1987 Chapin et al. 1988 NTP 1994 Somkuti et al. 1987a, 1987b). 

No studies addressing developmental or reproductive effects following acute inhalation exposure to aniline were located. However, because effects on development and reproduction arise after systemic uptake, oral administration of aniline can be considered for evaluating potential developmental and reproductive toxicity. Aniline (administered as aniline hydrochloride) readily crosses the placental barrier in rodents (Price et al. 1985). 

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