Glutathione S-Transferase Alpha Expressed in Porcine Sertoli Cells Is under the Control of Follicle-Stimulating Hormone and Testosterone1

Benbrahim‐Tallaa, Lamia; Tabone, Eric; Tosser‐Klopp, Gwenola; Hatey, François; Benahmed, Mohamed

doi:10.1095/biolreprod66.6.1734

Cited by 33 publications

(18 citation statements)

References 46 publications

(43 reference statements)

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“…Protein extracts (80 mg/well for GSTa, 100 mg/well for AR) were size fractionated on SDSpolyacrylamide gel (Benbrahim-Tallaa et al 2002b). The membranes were incubated with the rabbit polyclonal antiGSTa antibody diluted 1:1000 or the rabbit polyclonal anti-AR antibody diluted 1:100 in a solution of tris buffered saline (TBS) with 0 .…”

Section: Methodsmentioning

confidence: 99%

“…This gene is expressed in both Leydig and Sertoli cells (Benbrahim-Tallaa et al 2002b) and was reported to be under the control of androgens in Sertoli cells (Benbrahim-Tallaa et al 2002b). In utero flutamide treatment resulted in a decrease in GSTa mRNA levels in seminiferous tubules with a significant decrease observed at 2 mg/kg d (PZ0 .…”

Section: Effects Of In Utero Exposure To Flutamide On Sertoli Cell Gementioning

confidence: 97%

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Alterations of Sertoli cell activity in the long-term testicular germ cell death process induced by fetal androgen disruption

Benbrahim‐Tallaa¹,

Siddeek²,

Bözec³

et al. 2007

Journal of Endocrinology

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Fetal androgen disruption, induced by the administration of anti-androgen flutamide (0 . 4, 2, and 10 mg/kg day) causes a long-term apoptosis in testicular germ cells in adult male rat offspring. One of the questions raised by this observation is the role of the Sertoli cells in the adult germ cell apoptotic process. It is shown here that Sertoli cells originating from 15-day-old rats treated in utero with the anti-androgen (10 mg/kg d) did no longer protect adult germ cells against apoptosis. Indeed, untreated spermatocytes or spermatids exhibited increased (P!0 . 0001) active caspase-3 levels when co-cultured with Sertoli cells isolated from rat testes exposed in utero to the anti-androgen. This alteration of Sertoli cell functions was not due to modifications in the androgen signal in the adult (90-day-old) animals, since plasma testosterone and estradiol, androgen receptor expression, and androgentargeted cell number (e.g., Sertoli cells in the seminiferous tubules) were not affected by the fetal androgen disruption. In contrast, this inability of Sertoli cells to protect germ cells against apoptosis could be accounted for by the potential failure of Sertoli cell functions. Indeed, adult testes exposed in utero to anti-androgens displayed decreased levels of several genes mainly expressed in adult Sertoli cells (anti-Mullerian hormone receptor type II (AMHR2), Cox-1, cyclin D2, cathepsin L, and GSTa). In conclusion, fetal androgen disruption may induce alterations of Sertoli cell activity probably related to Sertoli cell maturation, which potentially leads to increased adult germ cell apoptosis.

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Section: Methodsmentioning

confidence: 99%

Section: Effects Of In Utero Exposure To Flutamide On Sertoli Cell Gementioning

confidence: 97%

Alterations of Sertoli cell activity in the long-term testicular germ cell death process induced by fetal androgen disruption

Benbrahim‐Tallaa¹,

Siddeek²,

Bözec³

et al. 2007

Journal of Endocrinology

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“…[91][92][93] Levels of these GSHsynthesizing enzymes can be altered by both estrogens 94,95 and testosterone. 96,97 GSH is typically reduced under conditions of enhanced oxidative stress due to the enhanced destruction of GSH in the process of neutralizing free radicals. 98,99 Estrogens appear to have direct potent antioxidant activity, 100,101 and so may prevent the early decline in GSH that occurs in males by contributing to antioxidant defense.…”

Section: Glutathionementioning

confidence: 99%

Contributions of the sympathetic nervous system, glutathione, body mass and gender to blood pressure increase with normal aging: influence of heredity

Kennedy

Rao

Botiglieri³

et al. 2005

J Hum Hypertens

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Body mass and sympathetic activity increase with aging and might underlie blood pressure (BP) elevation. Increased body mass index (BMI) may elevate BP by increasing sympathetic activity. Glutathione (GSH) can decrease BP, and declines with aging. We measured systolic (SBP) and diastolic BP, BMI, plasma (NE pl ) and urine norepinephrine (NE u ), and plasma GSH in n ¼ 204 twins across the age spectrum. BP correlated directly with BMI, NE pl , and NE u , but inversely with GSH. Age correlated with BP, BMI, NE pl , and NE u . BP, BMI, NE pl , and NE u were higher in older subjects than younger subjects, whereas GSH was lower with aging. In older subjects with high (above median) NE pl , SBP was 8 mmHg higher than in those of comparable age with low NE. In younger subjects with high GSH, BP was significantly lower than in younger subjects having low GSH. NE u was significantly reduced in young high-BMI subjects vs young low-BMI subjects. The heritability (h 2 ) of NE pl, NE u , and GSH ranged from B50 to B70%, and these biochemical quantities were considerably more heritable than BP. We conclude that increases in sympathetic activity contribute to aging-induced SBP elevations, especially in older females. GSH reductions apparently participate in aging-induced BP elevations, most strongly in males. BMI increases contribute to BP elevations, particularly in younger subjects. BMI elevations apparently raise BP mainly by peripheral mechanisms, with generally little sympathetic activation. Substantial h 2 for plasma GSH, NE, and urine NE suggests that such traits may be useful 'intermediate phenotypes' in the search for genetic determinants of BP.

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“…Less is known about GST regulation by hormones. Adrenocorticotrophic hormone (39), glucocorticoids (19, 33), growth hormones (54), thyroid hormones (TH) (6,11,31), and sex steroids (7,25,30) are able to modulate GST.Thyroid hormones, including thyroxine (T 4 ) and triiodothyronine (T 3 ), are essential during embryonic development and play critical roles in several physiological processes in adult organisms (36). It is agreed that most of the TH effects are mediated by nuclear action via a superfamily of ligand-modulated transcription factors that modify target gene transcription (36).…”

mentioning

confidence: 99%

Thyroid hormone and estradiol have overlapping effects on kidney glutathioneS-transferase-α gene expression

Faustino

Almeida

Pereira

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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Class GST (Gsta) represents an essential component of cellular antioxidant defense mechanisms in both the liver and the kidney. Estrogens and thyroid hormones (TH) play central roles in animal development, physiology, and behavior. Evidence of the overlapping functions of thyroid hormones and estrogens has been shown, although the molecular mechanisms are not always clear. We evaluated an interaction between TH and estradiol in regulating kidney Gsta expression and function. First, we observed that female mice expressed greater amounts of Gsta compared with males and showed an opposite pattern of expression in TR␤ knock-in mice. To further investigate these sex differences, hypothyroidism was induced by a 5-propyl-2-thiouracil diet, and hyperthyroidism was induced by daily T 3 injections. Hypothyroidism increased kidney Gsta expression in male mice but not in female mice, indicating that sex hormones could be influencing the regulation of Gsta by thyroid hormones. To analyze this hypothesis, ovariectomized females were subjected to hypo-and hyperthyroidism, which led to a male profile of Gsta expression. When hypo-or hyperthyroid ovariectomized mice were treated with 17␤-estradiol benzoate, we were able to confirm that estradiol was interfering with TH modulation; Gsta expression is increased by T 3 when estradiol is present and decreased by T 3 when estradiol is absent. Using proximal tubule cells, we also showed that estradiol and T 3 worked together to modulate Gsta expression in an overlapping fashion. In summary, 1) the sex difference in the basal expression of Gsta impacts the detoxification process, 2) kidney Gsta expression is regulated by TH in males and females but in opposite directions, and 3) T 3 and estradiol interact directly in renal proximal cells to regulate Gsta expression in females.triiodothyronine; proximal tubule; cross-talk; ovariectomy; estrogen GLUTATHIONE S-TRANSFERASES (GSTs) are a superfamily of ubiquitous dimeric detoxification isoenzymes that conjugate many substrates to reduced glutathione (GSH), including several xenobiotic and endogenous electrophiles (26). Mammalian cytosolic GSTs represent the largest family of such transferases and have been divided into seven different classes (␣, , , , , , and ) (2, 27, 28). The ␣-class of GST (GST␣) is found in several organs, such as the liver, kidney, lung, stomach, and gonads, some of which exhibit sexual dimorphism (35). In the liver, the important role played by GST in cellular detoxification and in many other known functions has already been well described (26). However, in other tissues, the role of GST is still not well characterized.It has been established that GST␣ is a biomarker of renal toxicity that aids in the detoxification of endogenous and exogenous compounds and in drug metabolism (2). Renal GST isoforms are differentially expressed along nephron segments; expression also depends on species. In the human kidney, GST␣ is found predominantly in the proximal convoluted tubule, and low levels of GST␣ have been detected in the...

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Glutathione S-Transferase Alpha Expressed in Porcine Sertoli Cells Is under the Control of Follicle-Stimulating Hormone and Testosterone1

Cited by 33 publications

References 46 publications

Alterations of Sertoli cell activity in the long-term testicular germ cell death process induced by fetal androgen disruption

Alterations of Sertoli cell activity in the long-term testicular germ cell death process induced by fetal androgen disruption

Contributions of the sympathetic nervous system, glutathione, body mass and gender to blood pressure increase with normal aging: influence of heredity

Thyroid hormone and estradiol have overlapping effects on kidney glutathioneS-transferase-α gene expression

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