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Suppressive effects of long-term exposure to P-nitrophenol on gonadal development, hormonal profile with disruption of tissue integrity, and activation of caspase-3 in male Japanese quail (Coturnix japonica).

Ahmed E, Nagaoka K, Fayez M, Abdel-Daim MM, Samir H, Watanabe G - Environ Sci Pollut Res Int (2015)

Bottom Line: Meanwhile, the pituitary LH did not significantly change.Consequently, it may reduce the sensitivity of the anterior pituitary gland to secrete LH.In conclusion, PNP induced profound endocrine disruption in the form of hormonal imbalance, induction of CASP3, and disruption of CLDN1 expression in the testis.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Veterinary Physiology, Department of Veterinary Medicine, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu, Tokyo, 183-8509, Japan, eman_ahmed@vet.suez.edu.eg.

ABSTRACT
P-Nitrophenol (PNP) is considered to be one of nitrophenol derivatives of diesel exhaust particles. PNP is a major metabolite of some organophosphorus compounds. PNP is a persistent organic pollutant as well as one of endocrine-disrupting compounds. Consequently, bioaccumulation of PNP potentiates toxicity. The objectives of the current study were to assess in vivo adverse effects of long-term low doses of PNP exposure on reproductive system during development stage. Twenty-eight-day-old male Japanese quails were orally administered different doses of PNP (0, 0.01, 0.1, 1 mg/kg body weight) daily for 2.5 months. Testicular histopathology, hormones, caspase-3 (CASP3), and claudin-1 (CLDN1) tight junction protein, as well as plasma hormones were analyzed. The results revealed that long-term PNP exposure caused testicular histopathological changes such as vacuolation of spermatogenic cell and spermatocyte with significant testicular and cloacal gland atrophy. PNP activated CASP3 enzyme that is an apoptosis-related cysteine peptidase. Besides, it disrupted the expression of CLDN1. Furthermore, a substantial decrease in plasma concentrations of luteinizing hormone (LH) and testosterone was observed after 2 and 2.5 months in the PNP-treated groups. Meanwhile, the pituitary LH did not significantly change. Site of action of PNP may be peripheral on testicular development and/or centrally on the hypothalamic-pituitary-gonadal axis through reduction of pulsatile secretion of gonadotrophin-releasing hormone. Consequently, it may reduce the sensitivity of the anterior pituitary gland to secrete LH. In conclusion, PNP induced profound endocrine disruption in the form of hormonal imbalance, induction of CASP3, and disruption of CLDN1 expression in the testis. Hence, it may hinder the reproductive processes.

No MeSH data available.


Related in: MedlinePlus

Plasma concentrations of the testosterone (a–e) and the LH (f–j) at the different times in the control and the PNP-treated Japanese quails (0.01, 0.1, or 1 mg/kg b.w.). Each bar represents the mean ± S.E.M. of five birds per group. *P < 0.05; **P < 0.01 compared with value for control quail
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Fig3: Plasma concentrations of the testosterone (a–e) and the LH (f–j) at the different times in the control and the PNP-treated Japanese quails (0.01, 0.1, or 1 mg/kg b.w.). Each bar represents the mean ± S.E.M. of five birds per group. *P < 0.05; **P < 0.01 compared with value for control quail

Mentions: Plasma concentrations of testosterone and LH in the PNP-treated birds showed significant decrease after 2 and 2.5 months as shown in Fig. 3. Plasma concentrations of the testosterone (Fig. 3a–e) were significantly lower in both the 0.1- and 1.0-mg/kg-treated groups when compared with the control group after 2 months (0.076 ± 0.02, 0.14 ± 0.07vs. 1.33 ± 0.17) and 2.5 months (0.33 ± 0.05, 0.44 ± 0.14 vs. 3.19 ± 0.68 ng/ml), respectively. Testosterone level starts to record nonsignificant decrease and fluctuation after 0.5 months of PNP exposure. Concurrently, plasma concentrations of LH were significantly lower in the low and the high dose (4.33 ± 0.25 and 3.69 ± 0.65 ng/ml, respectively) after 2 months when compared with the control birds (6.83 ± 0.25 ng/ml) (Fig. 3i). Furthermore, after 2.5 months, LH hormone was 3.40 ± 0.49 and 3.1 ± 0.24 in the mid- and the high group, respectively, when compared with 5.94 ± 0.5 for the control birds (Fig. 3j). The concentrations of LH in the pituitary homogenate after 2.5 months tend to be increased in the low and the mid-doses, meanwhile they tend to decrease in the highest dose of the PNP (Fig. 4a–e). Plasma corticosterone (Fig. 4f) did not significantly increase after 1 month in low, mid-, and high groups (61.80 ± 16.94, 60.87 ± 12.54, and 78.35 ± 17.29, respectively) when compared with the control group (50.98 ± 8.678). After 2 months of PNP administration, the plasma corticosterone tended to decrease in the mid- and the high-dose groups when compared with the control group (16.32 ± 6.2 and 22.48 ± 2.1 vs. 31.89 ± 3.05). Plasma ir-inhibin and testicular ir-inhibin did not significantly change (data not shown).Fig. 3


Suppressive effects of long-term exposure to P-nitrophenol on gonadal development, hormonal profile with disruption of tissue integrity, and activation of caspase-3 in male Japanese quail (Coturnix japonica).

Ahmed E, Nagaoka K, Fayez M, Abdel-Daim MM, Samir H, Watanabe G - Environ Sci Pollut Res Int (2015)

Plasma concentrations of the testosterone (a–e) and the LH (f–j) at the different times in the control and the PNP-treated Japanese quails (0.01, 0.1, or 1 mg/kg b.w.). Each bar represents the mean ± S.E.M. of five birds per group. *P < 0.05; **P < 0.01 compared with value for control quail
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4490174&req=5

Fig3: Plasma concentrations of the testosterone (a–e) and the LH (f–j) at the different times in the control and the PNP-treated Japanese quails (0.01, 0.1, or 1 mg/kg b.w.). Each bar represents the mean ± S.E.M. of five birds per group. *P < 0.05; **P < 0.01 compared with value for control quail
Mentions: Plasma concentrations of testosterone and LH in the PNP-treated birds showed significant decrease after 2 and 2.5 months as shown in Fig. 3. Plasma concentrations of the testosterone (Fig. 3a–e) were significantly lower in both the 0.1- and 1.0-mg/kg-treated groups when compared with the control group after 2 months (0.076 ± 0.02, 0.14 ± 0.07vs. 1.33 ± 0.17) and 2.5 months (0.33 ± 0.05, 0.44 ± 0.14 vs. 3.19 ± 0.68 ng/ml), respectively. Testosterone level starts to record nonsignificant decrease and fluctuation after 0.5 months of PNP exposure. Concurrently, plasma concentrations of LH were significantly lower in the low and the high dose (4.33 ± 0.25 and 3.69 ± 0.65 ng/ml, respectively) after 2 months when compared with the control birds (6.83 ± 0.25 ng/ml) (Fig. 3i). Furthermore, after 2.5 months, LH hormone was 3.40 ± 0.49 and 3.1 ± 0.24 in the mid- and the high group, respectively, when compared with 5.94 ± 0.5 for the control birds (Fig. 3j). The concentrations of LH in the pituitary homogenate after 2.5 months tend to be increased in the low and the mid-doses, meanwhile they tend to decrease in the highest dose of the PNP (Fig. 4a–e). Plasma corticosterone (Fig. 4f) did not significantly increase after 1 month in low, mid-, and high groups (61.80 ± 16.94, 60.87 ± 12.54, and 78.35 ± 17.29, respectively) when compared with the control group (50.98 ± 8.678). After 2 months of PNP administration, the plasma corticosterone tended to decrease in the mid- and the high-dose groups when compared with the control group (16.32 ± 6.2 and 22.48 ± 2.1 vs. 31.89 ± 3.05). Plasma ir-inhibin and testicular ir-inhibin did not significantly change (data not shown).Fig. 3

Bottom Line: Meanwhile, the pituitary LH did not significantly change.Consequently, it may reduce the sensitivity of the anterior pituitary gland to secrete LH.In conclusion, PNP induced profound endocrine disruption in the form of hormonal imbalance, induction of CASP3, and disruption of CLDN1 expression in the testis.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Veterinary Physiology, Department of Veterinary Medicine, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu, Tokyo, 183-8509, Japan, eman_ahmed@vet.suez.edu.eg.

ABSTRACT
P-Nitrophenol (PNP) is considered to be one of nitrophenol derivatives of diesel exhaust particles. PNP is a major metabolite of some organophosphorus compounds. PNP is a persistent organic pollutant as well as one of endocrine-disrupting compounds. Consequently, bioaccumulation of PNP potentiates toxicity. The objectives of the current study were to assess in vivo adverse effects of long-term low doses of PNP exposure on reproductive system during development stage. Twenty-eight-day-old male Japanese quails were orally administered different doses of PNP (0, 0.01, 0.1, 1 mg/kg body weight) daily for 2.5 months. Testicular histopathology, hormones, caspase-3 (CASP3), and claudin-1 (CLDN1) tight junction protein, as well as plasma hormones were analyzed. The results revealed that long-term PNP exposure caused testicular histopathological changes such as vacuolation of spermatogenic cell and spermatocyte with significant testicular and cloacal gland atrophy. PNP activated CASP3 enzyme that is an apoptosis-related cysteine peptidase. Besides, it disrupted the expression of CLDN1. Furthermore, a substantial decrease in plasma concentrations of luteinizing hormone (LH) and testosterone was observed after 2 and 2.5 months in the PNP-treated groups. Meanwhile, the pituitary LH did not significantly change. Site of action of PNP may be peripheral on testicular development and/or centrally on the hypothalamic-pituitary-gonadal axis through reduction of pulsatile secretion of gonadotrophin-releasing hormone. Consequently, it may reduce the sensitivity of the anterior pituitary gland to secrete LH. In conclusion, PNP induced profound endocrine disruption in the form of hormonal imbalance, induction of CASP3, and disruption of CLDN1 expression in the testis. Hence, it may hinder the reproductive processes.

No MeSH data available.


Related in: MedlinePlus