Normal Reproductive Organ Development in Wistar Rats Exposed to Bisphenol A in the Drinking Water

1999 ◽  
Vol 30 (2) ◽  
pp. 130-139 ◽  
Author(s):  
S.Z. Cagen ◽  
J.M. Waechter ◽  
S.S. Dimond ◽  
W.J. Breslin ◽  
J.H. Butala ◽  
...  
Keyword(s):  
Drinking Water ◽  
Bisphenol A ◽  
Wistar Rats ◽  
Reproductive Organ ◽  
Organ Development

Dose exposure of Bisphenol- A on female Wistar rats fertility

2019 ◽  
Vol 38 (2) ◽  
Author(s):  
Seema Srivastava ◽  
Nupoor Dhagga
Keyword(s):  
Bisphenol A ◽  
Wistar Rats ◽  
Environmental Pollutants ◽  
Reproductive Organs ◽  
Reproductive Organ ◽  
Fertility Rate ◽  
Organ Weight ◽  
Female Wistar Rats ◽  
Increased Sensitivity ◽  
Plastic Containers

Abstract Background 2, 2-Bis (4-hydroxyphenyl propane [bisphenol A (BPA)] is one of the major environmental pollutants and has the adverse effects on human health. BPA mimics the structure of estrogen and binds to estrogen receptors and alters the secretion of the hormone. It is ingested in humans through the regular use of plastic containers, bottles and food cans. Materials and methods Female Wistar rats were exposed orally to 5, 50, 300, 600 and 800 mg BPA/kg body weight (bd. wt.)/week mixed in olive oil and administered every 168 h for 3 months continuing through the mating, gestation and lactation and its effects on fertility, reproductive organ weight and hormones [LH (luteinizing hormone), FSH (follicle stimulating hormone), estradiol (E2), progesterone (PROG) and PRL (prolactin)] were evaluated. Results The findings revealed that females exposed to BPA exhibited a decrease in female fertility rate and weight of reproductive organs (ovary and uterus) with significant decreased levels of LH, FSH, E2, PROG and PRL in the non-pregnancy phase whereas in cesarean and post-term females, no significance difference was found in fertility rate, reproductive organ weight and hormonal levels. Conclusions These data indicate an increased sensitivity to BPA needs careful evaluation of the current levels of exposure.

scholarly journals Normal reproductive organ development in CF-1 mice following prenatal exposure to bisphenol A

1999 ◽  
Vol 50 (1) ◽  
pp. 36-44 ◽  
Author(s):  
S. Z. Cagen ◽  
J. M. Waechter ◽  
S. S. Dimond ◽  
W. J. Breslin ◽  
J. H. Butala ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Prenatal Exposure ◽  
Reproductive Organ ◽  
Organ Development

scholarly journals Bisphenol AF and Bisphenol F Induce Similar Feminizing Effects in Chicken Embryo Testis as Bisphenol A

2020 ◽  
Vol 178 (2) ◽  
pp. 239-250
Author(s):  
Anna Mentor ◽  
Mimmi Wänn ◽  
Björn Brunström ◽  
Maria Jönsson ◽  
Anna Mattsson
Keyword(s):  
Bisphenol A ◽  
Chicken Embryo ◽  
Reproductive Organ ◽  
Testis Size ◽  
Organ Development ◽  
Bisphenol S ◽  
Left Testis ◽  
Bisphenol F ◽  
Bisphenol Af ◽  
Somatic Index

Abstract The plastic component bisphenol A (BPA) impairs reproductive organ development in various experimental animal species. In birds, effects are similar to those caused by other xenoestrogens. Because of its endocrine disrupting activity, BPA is being substituted with other bisphenols in many applications. Using the chicken embryo model, we explored whether the BPA alternatives bisphenol AF (BPAF), bisphenol F (BPF), and bisphenol S (BPS) can induce effects on reproductive organ development similar to those induced by BPA. Embryos were exposed in ovo from embryonic day 4 (E4) to vehicle, BPAF at 2.1, 21, 210, and 520 nmol/g egg, or to BPA, BPF, or BPS at 210 nmol/g egg and were dissected on embryonic day 19. Similar to BPA, BPAF and BPF induced testis feminization, manifested as eg testis-size asymmetry and ovarian-like cortex in the left testis. In the BPS-group, too few males were alive on day 19 to evaluate any effects on testis development. We found no effects by any treatment on ovaries or Müllerian ducts. BPAF and BPS increased the gallbladder-somatic index and BPAF, BPF and BPS caused increased embryo mortality. The overall lowest-observed-adverse-effect level for BPAF was 210 nmol/g egg based on increased mortality, increased gallbladder-somatic index, and various signs of testis feminization. This study demonstrates that the BPA replacements BPAF, BPF, and BPS are embryotoxic and suggests that BPAF is at least as potent as BPA in inducing estrogen-like effects in chicken embryos. Our results support the notion that these bisphenols are not safe alternatives to BPA.

Insulin-induced endothelin release and vasoreactivity in hypertriglyceridemic and hypertensive rats

1999 ◽  
Vol 277 (1) ◽  
pp. H399-H404 ◽  
Author(s):  
Pilar Nava ◽  
Verónica Guarner ◽  
Rosalinda Posadas ◽  
Israel Pérez ◽  
Guadalupe Baños
Keyword(s):  
Drinking Water ◽  
Receptor Antagonist ◽  
Wistar Rats ◽  
Receptor Blocker ◽  
Hypertensive Rats ◽  
Contractile Responses ◽  
Femoral Arteries ◽  
Male Wistar Rats

Insulin-elicited endothelin release in hypertriglyceridemic, hypertensive, hyperinsulinemic (HTG) rats was shown. Weanling male Wistar rats were given 30% sucrose in their drinking water for 20–24 wk. In vitro contractions of aorta and femoral arteries were elicited with 40 mM KCl. Endothelin release induced with KCl plus 50 μU/ml insulin resulted in increases in contractile responses: 41 ± 5.9 and 57 ± 6% for control and 65.5 ± 6 and 95 ± 9% for HTG aortas and femoral arteries, respectively. The endothelin ETB-receptor blocker BQ-788 decreased responses to KCl + insulin by 39 ± 8 and 53 ± 5% in control and 48 ± 13 and 79 ± 3.5% in HTG aortas and femoral arteries, respectively. The ETA-receptor antagonist PD-151242 inhibited these responses by 12 ± 10 and 1 ± 9% in control and by 51.5 ± 9 and 58.5 ± 1% in HTG aortas and femoral arteries, respectively. These results suggest that endothelin may contribute to the hypertension in this model.

scholarly journals Prenatal Bisphenol A Exposure Induces Preneoplastic Lesions in the Mammary Gland in Wistar Rats

2007 ◽  
Vol 115 (1) ◽  
pp. 80-86 ◽  
Author(s):  
Milena Durando ◽  
Laura Kass ◽  
Julio Piva ◽  
Carlos Sonnenschein ◽  
Ana M. Soto ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Bisphenol A ◽  
Wistar Rats ◽  
Preneoplastic Lesions

scholarly journals Toxic effects of Cr(VI) in liver after administration in the drinking water to Wistar rats

2006 ◽  
Vol 164 ◽  
pp. S202
Author(s):  
A. Rafael ◽  
A. Almeida ◽  
I. Parreira ◽  
P. Santos ◽  
M. Carvalho ◽  
...  
Keyword(s):  
Drinking Water ◽  
Wistar Rats ◽  
Toxic Effects

Determination of the L-ascorbic acid requirements in Wistar osteogenic disorder Shionogi rats for prolonged carcinogenesis experiments

1996 ◽  
Vol 30 (4) ◽  
pp. 337-346 ◽  
Author(s):  
S. W. Y. Chan ◽  
P. C. Reade
Keyword(s):  
Animal Model ◽  
Ascorbic Acid ◽  
Drinking Water ◽  
Normal Level ◽  
Physical Condition ◽  
Wistar Rats ◽  
Clinical Signs ◽  
Supplement Group ◽  
Palatal Mucosa

Wistar Shionogi rats of the ( od/od) substrain with the osteogenic disorder are unable to synthesize L-ascorbic acid ( L-AA) and appear to be an appropriate animal model for studying the effect of L-AA in carcinogenesis. To determine the minimal L-AA requirements of these animals for prolonged survival in a satisfactory physical condition during experimentation, four concentrations of L-AA (0.33 g/l, 0.67 g/l, 1.67 g/l and 3.33 g/l) were administered via drinking water to four groups of animals ( n=2). Their water intake per cage was recorded three times weekly and the plasma L-AA levels were determined at the start, after 2, 4, 8 and 12 weeks and at the termination of the experiment. To simulate the procedures to be undertaken in oral mucosal carcinogenesis experiments, the animals were gently restrained and a designated amount of sterile NaCl was applied to the palatal mucosa three times a week for 26 weeks. The L-AA supplement group with the lowest concentration (0.33 g/l L-AA) achieved mean plasma levels of 7 ± 1.38 μM, approximately one-eighth that of the normal level (mean plasma L-AA level in outbred Wistar rats was found to be 58 ± 3 μM) whilst those in the higher supplement group (3.33 g/l L-AA) achieved a mean of 18 ± 1.25 μM. All of the animals employed in the present study survived for 26 weeks and showed no clinical signs of L-AA deficiency during this period.

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