Differential effects of temperature on reactive oxygen/nitrogen species production in rat pachytene spermatocytes and round spermatids

Pino, José A.; Osses, Nelson; Oyarzún, Daniela; Farías, Jorge G.; Moreno, Ricardo D.; Reyes, Juan G.

doi:10.1530/rep-12-0330

Cited by 19 publications

(13 citation statements)

References 32 publications

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“…The ROS and their derived reactive nitrogen species have been characterized as the main contributors to cell death in hyperthermia (43). In this study, we correlated the cold response to an increase in both [ROS] and apoptosis of spermatocytes.…”

Section: Discussionmentioning

confidence: 99%

Cold/menthol TRPM8 receptors initiate the cold‐shock response and protect germ cells from cold‐shock–induced oxidation

et al. 2016

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Testes of most male mammals present the particularity of being externalized from the body and are consequently slightly cooler than core body temperature (4–8°C below). Although, hypothermia of the testis is known to increase germ cells apoptosis, little is known about the underlying molecular mechanisms, including cold sensors, transduction pathways, and apoptosis triggers. In this study, using a functional knockout mouse model of the cold and menthol receptors, dubbed transient receptor potential melastatine 8 (TRPM8) channels, we found that TRPM8 initiated the cold-shock response by differentially modulating cold- and heat-shock proteins. Besides, apoptosis of germ cells increased in proportion to the cooling level in control mice but was independent of temperature in knockout mice. We also observed that the rate of germ cell death correlated positively with the reactive oxygen species level and negatively with the expression of the detoxifying enzymes. This result suggests that the TRPM8 sensor is a key determinant of germ cell fate under hypothermic stimulation.—Borowiec, A.-S., Sion, B., Chalmel, F., Rolland, A. D., Lemonnier, L., De Clerck, T., Bokhobza, A., Derouiche, S., Dewailly, E., Slomianny, C., Mauduit, C., Benahmed, M., Roudbaraki, M., Jégou, B., Prevarskaya, N., Bidaux, G. Cold/menthol TRPM8 receptors initiate the cold-shock response and protect germ cells from cold-shock–induced oxidation.

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Section: Discussionmentioning

confidence: 99%

Cold/menthol TRPM8 receptors initiate the cold‐shock response and protect germ cells from cold‐shock–induced oxidation

et al. 2016

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“…For normal spermatogenesis, generation of ROS during heat stress and involvement in spermatogenic cell damage are common [35][36][37]. In this context, it is not surprising to see the up-regulation of YES1 expression and activity in PS, as these cells are more susceptible to oxidative stress at high temperatures (408C) [38].…”

Section: Discussionmentioning

confidence: 99%

YES1 Activation Elicited by Heat Stress Is Anti-Apoptotic in Mouse Pachytene Spermatocytes1

Liang¹,

Dong²,

Zhao³

et al. 2013

Biology of Reproduction

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Deregulated expression of protein tyrosine phosphorylation has been implicated in testicular response to different stimuli. Herein, YES1, a nonreceptor protein tyrosine kinase, was found to be significantly up-regulated in pachytene spermatocytes (PS) during early recovery from a transient testicular heat stress. Coculture of PS with Sertoli cells (SCs) could enhance the hyperthermia-induced YES1 activation, indicative of a positive regulation of the paracrine signaling. Moreover, SU6656, a selective YES1 inhibitor, was shown to effectively block YES1 activity, thereafter resulting in a dramatic increase of heat stress-induced apoptosis in primary cultured PS. Mechanistically, the antiapoptotic effect of YES1 activation in response to testicular heat insult may mediate via the regulation of extracellular signal-regulated kinase (ERK)/metastasis-associated 1 (MTA1) cascade. From a clinical standpoint, a notably higher level of YES1 expression was observed in the pathological testis from varicocele patients as compared to a negligible staining in the control group. Taken together, our present results provide the first evidence that the YES1/ERK/MTA1/p53 cascade may serve as a naturally occurring, indispensable self-defensive mechanism maintaining apoptotic balance during meiotic heat stress. Our study may have also partially answered the question of how activation of signal pathways at the cell membrane surface interacts with the key regulatory events occurring in the nucleus during testicular heat shock.

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“… 14 15 Experimental models have also shown that transient mild testicular hyperthermia can destroy the balance between oxidative capacity and antioxidant capacity. 16 17 The human spermatozoa are highly susceptible to oxidative stress, high levels of free radicals, and reactive oxygen species (ROS), including the superoxide anion and hydrogen peroxide (H 2 O 2 ). 18 19 Oxidative stress can be deleterious and cause oxidative damage to the sperm plasma membrane and DNA fragmentation of both the nuclear and mitochondrial genomes.…”

Section: Introductionmentioning

confidence: 99%

Effect of transient scrotal hyperthermia on sperm parameters, seminal plasma biochemical markers, and oxidative stress in men

et al. 2015

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In this experimental prospective study, we aimed to analyze the effect of transient scrotal hyperthermia on the male reproductive organs, from the perspective of sperm parameters, semen plasma biochemical markers, and oxidative stress, to evaluate whether different frequencies of heat exposure cause different degrees of damage to spermatogenesis. Two groups of volunteers (10 per group) received testicular warming in a 43°C water bath 10 times, for 30 min each time: group 1: 10 consecutive days; group 2: once every 3 days. Sperm parameters, epididymis and accessory sex gland function, semen plasma oxidative stress and serum sex hormones were tested before treatment and in the 16-week recovery period after treatment. At last, we found an obvious reversible decrease in sperm concentration (P = 0.005 for Group 1 and P= 0.008 for Group 2 when the minimums were compared with baseline levels, the same below), motility (P = 0.009 and 0.021, respectively), the hypoosmotic swelling test score (P = 0.007 and 0.008, respectively), total acrosin activity (P = 0.018 and 0.009, respectively), and an increase in the seminal plasma malondialdehyde concentration (P = 0.005 and 0.017, respectively). The decrease of sperm concentration was greater for Group 2 than for Group 1 (P = 0.031). We concluded that transient scrotal hyperthermia seriously, but reversibly, negatively affected the spermatogenesis, oxidative stress may be involved in this process. In addition, intermittent heat exposure more seriously suppresses the spermatogenesis compared to consecutive heat exposure. This may be indicative for clinical infertility etiology analysis and the design of contraceptive methods based on heat stress.

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Differential effects of temperature on reactive oxygen/nitrogen species production in rat pachytene spermatocytes and round spermatids

Cited by 19 publications

References 32 publications

Cold/menthol TRPM8 receptors initiate the cold‐shock response and protect germ cells from cold‐shock–induced oxidation

Cold/menthol TRPM8 receptors initiate the cold‐shock response and protect germ cells from cold‐shock–induced oxidation

YES1 Activation Elicited by Heat Stress Is Anti-Apoptotic in Mouse Pachytene Spermatocytes1

Effect of transient scrotal hyperthermia on sperm parameters, seminal plasma biochemical markers, and oxidative stress in men

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