scholarly journals Effects of benzene, quercetin, and their combination on porcine ovarian cell proliferation, apoptosis, and hormone release

2019 ◽  
Vol 62 (1) ◽  
pp. 345-351 ◽  
Author(s):  
Adam Tarko ◽  
Aneta Štochmal'ová ◽  
Katarína Jedličková ◽  
Sandra Hrabovszká ◽  
Adriana Vachanová ◽  
...  

Abstract. We hypothesized that the environmental contaminant benzene and the plant antioxidant quercetin may affect ovarian cell functions and that quercetin could offer protection against the adverse effects of benzene. This study aimed to examine the action of benzene, quercetin, and their combination on porcine ovarian granulosa cell functions. We elucidated the effects of benzene (20 µg mL−1), quercetin (at the doses 0, 1, 10, 100 µg mL−1), and their combination on ovarian granulosa cell functions (proliferation, apoptosis, and hormone release) in vitro using immunocytochemistry and enzyme immunoassay respectively. Benzene alone stimulated proliferation, apoptosis, and oxytocin release and inhibited progesterone and prostaglandin F release. Quercetin alone inhibited proliferation, apoptosis, and stimulated oxytocin release but did not affect progesterone and prostaglandin F release. When used in combination with benzene, quercetin promoted the inhibitory effect of benzene on progesterone release. Overall, these data suggest that benzene and quercetin have direct stimulatory and inhibitory effects, respectively, on basic ovarian functions. Moreover, no protective action of quercetin against the effects of benzene was found. Rather, it was found to enhance the effect of benzene on progesterone release. Therefore, quercetin cannot be considered for preventing or mitigating the effects of benzene on reproductive processes.

2019 ◽  
Vol 44 (5) ◽  
pp. 507-511
Author(s):  
Aneta Štochmal’ová ◽  
Abdel Halim Harrath ◽  
Saleh Alwasel ◽  
Alexander V. Sirotkin

Flaxseed is useful as a functional food and alternative medicine owing to its beneficial health effects. Its action on ovarian cell functions and interrelationships with the upstream hormonal regulators remain unknown. Our aim was to examine the direct influence of flaxseed extract on basal porcine ovarian functions (proliferation, apoptosis), leptin release, and response to insulin-like growth factor I (IGF-I). First, we examined the effect of flaxseed extract on the accumulation of proliferation (PCNA) and apoptosis (Bax) markers and on leptin release in cultured porcine ovarian granulosa cells. Next, granulosa cells were cultured with IGF-I with and without flaxseed extract and analyzed for PCNA and Bax accumulation by quantitative immunocytochemistry and for leptin release by radioimmunoassay. Flaxseed decreased the accumulation of PCNA and increased that of Bax at all doses and reduced leptin output at 100 μg/mL. In contrast, IGF-I promoted PCNA accumulation and suppressed Bax. Flaxseed did not modify IGF-I action on these parameters. Thus, we showed that flaxseed influences porcine reproductive processes, having a direct effect on the ovary and the ability to affect ovarian cell proliferation, apoptosis, and leptin release. Furthermore, we confirmed the pro-proliferative and antiapoptotic actions of IGF-I but showed that flaxseed action on ovarian cell proliferation and apoptosis is not due to changes in the cell response to IGF-I. The potential direct anti-reproductive action of flaxseed needs to be considered during its application in nutrition, medicine, and animal production.


2019 ◽  
Vol 54 (6) ◽  
pp. 533-537 ◽  
Author(s):  
Adriana Kolesarova ◽  
Shubhadeep Roychoudhury ◽  
Bibiana Klinerova ◽  
Dagmara Packova ◽  
Katarina Michalcova ◽  
...  

2017 ◽  
Vol 234 (1) ◽  
pp. 1-14 ◽  
Author(s):  
Li Zhang ◽  
XiaoXin Zhang ◽  
Xuejing Zhang ◽  
Yu Lu ◽  
Lei Li ◽  
...  

MicroRNAs (MiRNAs) play important regulatory roles in many cellular processes. MiR-143 is highly enriched in the mouse ovary, but its roles and underlying mechanisms are not well understood. In the current study, we show that miR-143 is located in granulosa cells of primary, secondary and antral follicles. To explore the specific functions of miR-143, we transfected miR-143 inhibitor into primary cultured granulosa cells to study the loss of function of miR-143 and the results showed that miR-143 silencing significantly increased estradiol production and steroidogenesis-related gene expression. Moreover, our in vivo and in vitro studies showed that follicular stimulating hormone (FSH) significantly decreased miR-143 expression. This function of miR-143 is accomplished by its binding to the 3’-UTR of KRAS mRNA. Furthermore, our results demonstrated that miR-143 acts as a negative regulating molecule mediating the signaling pathway of FSH and affecting estradiol production by targeting KRAS. MiR-143 also negatively acts in regulating granulosa cells proliferation and cell cycle-related genes expression. These findings indicate that miR-143 plays vital roles in FSH-induced estradiol production and granulosa cell proliferation, providing a novel mechanism that involves miRNA in regulating granulosa cell functions.


2020 ◽  
Vol 14 (5) ◽  
pp. 683-695 ◽  
Author(s):  
Alexander V. Sirotkin ◽  
Monika Radosová ◽  
Adam Tarko ◽  
Iris Martín-García ◽  
Francisco Alonso

2009 ◽  
Vol 110 (1) ◽  
pp. 95-106 ◽  
Author(s):  
Craig N. Harvey ◽  
Mahmoud Esmail ◽  
Qi Wang ◽  
Andrew I. Brooks ◽  
Rob Zachow ◽  
...  

1986 ◽  
Vol 109 (3) ◽  
pp. 393-397 ◽  
Author(s):  
K. T. O'Byrne ◽  
L. Eltringham ◽  
G. Clarke ◽  
A. J. S. Summerlee

ABSTRACT The effect of relaxin on electrically evoked release of oxytocin from the posterior pituitary was examined by monitoring changes in intramammary pressure in the anaesthetized lactating rat. The amount of oxytocin released by electrical stimulation of the neurohypophysis in vivo was dramatically reduced following i.v. injection of highly purified porcine relaxin (2·5–10 μg/rat). Relaxin inhibited oxytocin release in a dose-dependent manner and the onset of inhibition occurred within 6–10 min and lasted for 10–60 min. No effect on the sensitivity of the mammary gland to exogenous oxytocin was observed after relaxin treatment. During the period of inhibition, i.v. injection of the opioid antagonist naloxone chloride (1 mg/kg) completely and immediately restored electrically evoked oxytocin release. The neurohypophysis is known to contain endogenous opioid peptides, therefore the effect of relaxin on electrically stimulated release of oxytocin from the rat isolated neural lobe in vitro was examined. Relaxin (500–2000 ng/ml) failed to inhibit oxytocin release in vitro. The results suggest that relaxin can inhibit the release of oxytocin from terminals in the neurohypophysis, but by an indirect mechanism. This action appears to be mediated through endogenous opioid peptides whose source is not clear. They are unlikely to be of neurohypophysial origin and may probably come from the adrenal medulla, since acute adrenalectomy negated the inhibitory effect of relaxin on oxytocin release. J. Endocr. (1986) 109, 393–397


1977 ◽  
Vol 162 (1) ◽  
pp. 9-18 ◽  
Author(s):  
L Å Idahl ◽  
Å Lernmark ◽  
J Sehlin ◽  
I B Täljedal

Exposing micro-dissected pancreatic islets of non-inbred ob/ob mice to 2-5 mM-alloxan for 10 min decreased the ability of the islets to accumulate Rb+. Rb+ accumulation in pieces of exocrine pancreas was unaffected by alloxan. When islets were treated with alloxan in the presence of 2-20 mM-D-glucose, the Rb+-accumulating ability was protected in a dose-dependent manner. The protective action of D-glucose was reproduced with 3-O-methyl-D-glucose but not with L-glucose or D-mannoheptulose; mannoheptulose prevented D-glucose from exerting its protective action. The inhibition of Rb+ accumulation was due to a decreased inward pumping, since alloxan did not affect Rb+ efflux from pre-loaded islets. The inhibitory effect of alloxan had a latency of about 1 min, as revealed by experiments with dispersed islet cells in suspension. Alloxan-treated islets showed only a marginal decrease in ATP and no change in glucose 6-phosphate concentration. Although alloxan slightly decreased the hydrolysis of ATP in a subcellular fraction enriched in plasma membranes, this effect could not be attributed to a ouabain-sensitive adenosine triphosphatase. The plasma membranes exhibited a K+-activated hydrolysis of p-nitrophenyl phosphate; this enzyme activity too was insensitive to alloxan. Glucose may protect the univalent-cation pump by preventing permeation of alloxan via a path coupled to the hexose-transport system. Inhibition of the pump may be fundamental to the induction of alloxan-diabetes.


1975 ◽  
Vol 67 (3) ◽  
pp. 453-458 ◽  
Author(s):  
R. E. J. DYBALL

SUMMARY Isolated rat neural lobes were incubated in vitro in Locke's solution containing anaesthetic quantities of urethane, pentobarbitone or tribromoethanol. The oxytocin content of the incubation medium was estimated before, during and after stimulation of the tissue by raising the potassium chloride concentration from 5·6 to 56 mmol/l. Urethane (25 mmol/l) significantly potentiated oxytocin release (P < 0·01) whereas tribromoethanol (0·5 mmol/l) had no obvious effect and pentobarbitone (0·4 mmol/l) significantly (P < 0·01) inhibited its release. Reduction of the sodium chloride concentration in the medium potentiated the release of oxytocin in each case but did not alter its pattern. Urethane which increased secretion of oxytocin also increased calcium ion uptake by the neural lobes and pentobarbitone which decreased oxytocin release decreased calcium ion uptake. The results may explain why the blood concentration of the neurohypophysial hormones tends to be higher in rats anaesthetized with urethane than with tribromoethanol. Inhibition of hormone release by pentobarbitone suggests that this anaesthetic is unsuitable for use in studies of neurohypophysial hormone release. A partial explanation of the anaesthetic properties of urethane and pentobarbitone may also have been found if the release of neurotransmitter substances is influenced in a similar manner.


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