| Full text | |
| Author(s): |
Tenorio, Bruno Mendes
[1]
;
da Silva, Reginaldo Pereira
[2]
;
Angelo Mendes Tenorio, Fernanda das Chagas
[2]
;
Costa Rosales, Roberta Ribeiro
[3]
;
da Silva Junior, Valdemiro Amaro
[4]
;
Nogueira, Romildo de Albuquerque
[4]
Total Authors: 6
|
| Affiliation: | [1] Univ Fed Paraiba, Hlth Sci Ctr, Dept Morphol, Joao Pessoa, Paraiba - Brazil
[2] Univ Fed Pernambuco, Biosci Ctr, Recife, PE - Brazil
[3] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Physiol, Ribeirao Preto, SP - Brazil
[4] Univ Fed Rural Pernambuco, Dept Anim Morphol & Physiol, Recife, PE - Brazil
Total Affiliations: 4
|
| Document type: | Journal article |
| Source: | Journal of Thermal Biology; v. 84, p. 1-7, AUG 2019. |
| Web of Science Citations: | 0 |
| Abstract | |
Heat can trigger testicular damage and impair fertility. Leydig cells produce testosterone in response to stimulation by luteinizing hormone (LH), which induces Ca2+ entry and K+ efflux through ion channels in their plasma membrane. Considering that mechanisms coordinating the Leydig cell responses to hyperthermic stress remain unclear; the present study analyzed the effects of heat stress (HS, 43 degrees C, 15 min) and inhibition of Hsp90 on T-type calcium currents and voltage-dependent potassium currents (VKC) in mice Leydig cells. Results show that HS reduced the VKC steady state currents at +80 mV (45.3%) and maximum conductance (71.5%), as well as increased the activation time constant (31.7%) and the voltage for which half the channels are open (30%). Hsp90 inhibition did not change the VKC currents. T-type calcium currents were not affected by HS or Hsp90 inhibition. In conclusion, HS can slow the activation, reduce the currents and voltage dependence of the VKC, suggesting a possible role of these currents in the response to hyperthermic stress in Leydig cells. (AU) | |
| FAPESP's process: | 10/16600-9 - Calcium handling and secretion in Leydig cells |
| Grantee: | Wamberto Antonio Varanda |
| Support Opportunities: | Regular Research Grants |