Hypophysectomy and/or peroxisome proliferators strongly influence the levels of phase II xenobiotic metabolizing enzymes in rat testis

Mehrotra, Kalika; Morgenstern, Ralf; Ahlberg, Margot Bengtsson; Georgellis, Antonis

doi:10.1016/s0009-2797(99)00110-6

Cited by 10 publications

(6 citation statements)

References 24 publications

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“…The majority of the cytosolic GPx in rat testis existed as selenium- and nonselenium-dependent GPx which is present in the Leydig cells. Much lower levels are associated in sertoli and spermatogenetic cells [54]. GPx is primarily responsible for H 2 O 2 removal in testicular mitochondria that does not contain catalase.…”

Section: Discussionmentioning

confidence: 99%

“…GPx plays a crucial role in scavenging peroxyl radicals and thereby maintains functional integrity of the cell membrane, spermatogenesis, sperm morphology, and motility [55]. In testis, PH-GPx or GPx-4 which is partially cytosolic and partially bound to nuclei and mitochondria is localized within maturating spermatogenetic cells [54]. Gpx-1 has mitochondrial and cytosolic subcellular localizations in all mammalian tissues [56].…”

Section: Discussionmentioning

confidence: 99%

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Compromised Rat Testicular Antioxidant Defence System by Hypothyroidism before Puberty

Sahoo

Roy

2012

International Journal of Endocrinology

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Altered thyroid function during early stages of development is known to affect adversely testicular growth, physiology, and antioxidant defence status at adulthood. The objective of the present study is to investigate the modulation of antioxidant defence status in neonatal persistent hypothyroid rats before their sexual maturation and also to identify the specific testicular cell populations vulnerable to degeneration during neonatal hypothyroidism in immature rats. Hypothyroidism was induced in neonates by feeding the lactating mother with 0.05% 6-n-propyl-2-thiouracil (PTU) through the drinking water. From the day of parturition till weaning (25 day postpartum), the pups received PTU through mother's milk (or) drinking water and then directly from drinking water containing PTU for the remaining period of experimentation. On the 31st day postpartum, the animals were sacrificed for the study. An altered antioxidant defence system marked by elevated SOD, CAT, and GR activities, with decreased GPx and GST activities were observed along with increased protein carbonylation, disturbed redox status in hypothyroid immature rat testis. This compromised testicular antioxidant status might have contributed to poor growth and development by affecting the spermatogenesis and steroidogenesis in rats before puberty as indicated by reduced germ cell number, complete absence of round spermatids, decreased seminiferous tubule diameter, and decreased testosterone level.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Compromised Rat Testicular Antioxidant Defence System by Hypothyroidism before Puberty

Sahoo

Roy

2012

International Journal of Endocrinology

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“…Adult rats treated with 0.05− 0.5% PFOA exhibited reduced activities of testicular-metabolic enzymes. 4,5 While chronic exposure of adult rats to PFDA (0.2, 0.5 mg•kg −1 •day −1 ) resulted in disruption of testicular steroidogenesis. 6 Using microsomal preparations of human and rat testes, PFCs were found to target on the steroidogenic enzyme (i.e., 3β-hydroxysteroid dehydrogenase) to reduce testosterone production.…”

Section: ■ Introductionmentioning

confidence: 99%

Comparative Analysis of PFOS and PFOA Toxicity on Sertoli Cells

Wan

Lai

Wong

2020

Environ. Sci. Technol.

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Perfluoroalkyl chemicals induce male reproductive toxicity. Current evidence showed the effects of the chemical exposure on the deterioration of testicular functions, and reduction in epididymal sperm counts. Previous studies showed that PFOA and PFOS displayed a high correlation with each other in seminal plasma levels, but induced different effects on semen variables. In this study, we focused on the comparative toxicity analysis of PFOA and PFOS, using a rat primary Sertoli cell model. Our transcriptomic data showed that PFOA and PFOS treatments (40 μM) perturbed global gene expression. While PFOS induced higher toxicity in affecting cytoskeleton signaling, Sertoli cell−cell junction, and inflammation, underlined by Ingenuity pathway analysis. Immunocytochemical staining revealed that PFOS treatment (40 and 80 μM) induced truncated actin filament and disorganized bundled configuration in the cell cytoplasm. Moreover, disorganized distribution of N-cadherin (N-cad) and β-catenin (β-cat), and defragmentation of ZO-1 at the Sertoli cell− cell interface was evident. At 80 μM of PFOS, cytoplasmic distribution of N-cad, β-cat, and ZO-1 were observed. We then examined whether resveratrol, a polyphenol antioxidant, was able to protect the cells from PFOS toxicity. The pretreatment of Sertoli cells with 10 μM resveratrol prevented the formation of truncated actin filament and dis-localization of β-cat. Western blot analysis showed that Res pretreatment increased the levels of basal ES proteins (N-cad and β-cat), tight junction proteins (ZO-1 and occludin), and gap junction protein, versus control.

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“…These results show that there were similar levels of antioxidant enzyme activity in hyperthyroid rats. It was reported that GPx activity was elevated but that SOD and catalase activities were lower in the testicular mitochondrial fractions obtained from hypothyroid rats (Mehrotra et al, 1999). The possible involvement of DBP-induced oxidative stress on testicular damage was determined by comparing the activity of the antioxidant enzymes (SOD, CAT, and GPx) in hyperthyroid (T3 þ DBP) rats.…”

Section: Discussionmentioning

confidence: 99%

“…This study is the first to report a relationship between testicular damage and the antioxidant status induced by DBP against thyroid hormone dysfunction. It reported that peroxisomes are present in the testes (Corton and Lapinskas, 2005), and peroxisome proliferators (PPs) in rat testicular cells can affect the antioxidant enzymes that protect them against oxidative stress (Mehrotra et al, 1999). Generally, CAT is located mainly in the peroxisomes and is induced by PPs in the liver and testis.…”

Section: Discussionmentioning

confidence: 99%

Effect of di(n‐butyl) phthalate on testicular oxidative damage and antioxidant enzymes in hyperthyroid rats

Lee

Ahn

Kim

et al. 2007

Environmental Toxicology

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This study compared the effects of di(n-butyl) phthalate (DBP) on the oxidative damage and antioxidant enzymes activity in testes of hyperthyroid rats. Hyperthyroidism was induced in pubertal male rats by intraperitoneal injection of triiodothyronine (T3, 10 microg/kg body weight) for 30 days. An oral dose of DBP (750 mg/kg) was administered simultaneously to normal or hyperthyroid (T3) rats over a 30-day period. No changes in body weight were observed in the hyperthyroid groups (T3, T3 + DBP) compared with controls. There were significantly higher serum T3 levels observed in the hyperthyroid rats than in the control, but the serum thyroid stimulating hormone levels were markedly lower in the hyperthyroid rats. DBP significantly decreased the weight of the testes in the normal (DBP) and hyperthyroid (T3 + DBP) groups. The serum testosterone concentrations were significantly lower in only DBP group. DBP significantly increased the 8-hydroxy-2-deoxyguanosine (8-OHdG) level in the testes, whereas the DBP-induced 8-OHdG levels were slightly higher in T3 + DBP group. Superoxide dismutase and glutathione peroxidase activities were significantly higher in the testes of the DBP or T3 + DBP groups. Catalase (CAT) activity was significantly higher in the DBP treatment group, but the T3 + DBP group showed slightly lower DBP-induced CAT activity. The testicular expression of thyroid hormone receptor alpha-1 (TRalpha-1) was significantly higher in the DBP groups, and androgen receptor (AR) expression was not detected in the DBP treatment group. In addition, DBP significantly increased the peroxisome proliferator-activated receptor-r (PPAR-r) levels in the testis. These results suggest that hyperthyroidism can cause a change in the expression level of PPAR-r in testes, and may increase the levels of oxidative damage induced by the metabolic activation of DBP.

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Hypophysectomy and/or peroxisome proliferators strongly influence the levels of phase II xenobiotic metabolizing enzymes in rat testis

Cited by 10 publications

References 24 publications

Compromised Rat Testicular Antioxidant Defence System by Hypothyroidism before Puberty

Compromised Rat Testicular Antioxidant Defence System by Hypothyroidism before Puberty

Comparative Analysis of PFOS and PFOA Toxicity on Sertoli Cells

Effect of di(n‐butyl) phthalate on testicular oxidative damage and antioxidant enzymes in hyperthyroid rats

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