Reactive oxygen species and male reproductive hormones

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hypogonadism 2 endocrinologydiseases
obesity 6 endocrinologydiseases
testosterone 77 endocrinologydiseasesdrugs
cortisol 9 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
cortisol 7000 male reproductive hormones. b Through the HPA axis, ROS increases the release of the stress hormone cortisol , which through the HPA-HPG axes cross-talk, further decreases LH secretion. c Elevated ROS also affects
cortisol 13341 on male reproductive hormonesExogenous sources Psychological stressBy increasing stress hormone ( cortisol ) levels and activating the immune–inflammatory systemDecreases serum testosterone and LH levels by
cortisol 16646 parameters [[51]–[53]]. It was reported that psychological stress can increase the circulating levels of cortisol and norepinephrine [[54]]. These hormones have a significant impact on increasing intracellular levels
cortisol 17290 [[56]]. Psychological stress can also increase the serum levels of corticosterone (in animals) and cortisol (in humans), which then enhance the apoptotic frequency of Leydig cells [[57]]. Furthermore, during
cortisol 19742 heat stress leads to a decline in the circulating levels of testosterone and LH but increases serum cortisol levels [[73], [74]]. Testicular heat stress also leads to Leydig cell apoptosis and a reduction in testosterone
cortisol 21307 chemicals’ (EDCs) that interfere with normal hormonal functions [[90]], enhance the level of circulating cortisol owing to OS induction [[91]] and reduces circulating testosterone levels [[92], [93]]. Increased cortisol
cortisol 21413 cortisol owing to OS induction [[91]] and reduces circulating testosterone levels [[92], [93]]. Increased cortisol decreases LH secretion through crosstalk between the HPG-HPA axes. Decreased LH concentration fails
cortisol 22952 adrenocorticotropic hormone (ACTH) secretion from the anterior pituitary thereby increasing the production of cortisol from adrenal cortex [[104]]. These radiations can also decrease testosterone secretion from Leydig cells
cortisol 41321 the generation of ROS, the HPA axis becomes activated and releases corticosterone (in animals) and cortisol (in humans) in response to stress. These stress hormones, through the cross-talk between the HPG and
testosterone 5158 membrane of Sertoli cells, while those of LH are on the Leydig cells. They coordinate to synthesize testosterone , maintain normal spermatogenesis, sperm health and density [[19]–[21]].Moreover, other hormones like
testosterone 5617 (Fig. 1). PRL-inhibiting GnRH secretion via modulation of dopaminergic pathway may also reduce LH and testosterone level and thus is associated with hypogonadism [[22]]. Dehydroepiandrosterone (DHEA) is another male
testosterone 6085 melatonin (MLT), a tryptophan-derived hormone of the pineal gland, positively regulates gonadotropin and testosterone secretion, and thus aid male reproductive functions [[26], [27]]. Anti-Mullerian hormone (AMH), a dimeric
testosterone 6448 ducts during the first 8 weeks of embryogenesis. It reflects Sertoli cell functions and is inhibited by testosterone under the influence of LH [[28]–[30]]. Interactions between the hypothalamo-pituitary-thyroid (HPT)
testosterone 7265 production from the thyroid gland, which through the cross-talk between HPT and HPG axes, again decreases testosterone synthesis. ROS also affects the other endocrine glands which interfere with these endocrine axes to
testosterone 7398 affects the other endocrine glands which interfere with these endocrine axes to result in decreased testosterone production. Increased oxidative stress (OS), in different conditions, decreases insulin production from
testosterone 7634 again reduces T3 production from the thyroid gland and through HPT-HPG axes cross-talk decreases testosterone biosynthesis. ROS production in obesity also increases circulating leptin levels which directly reduces
testosterone 7751 biosynthesis. ROS production in obesity also increases circulating leptin levels which directly reduces testosterone synthesis in the testis. Reduced melatonin in OS, and increased production of pro-inflammatory cytokines
testosterone 7939 of pro-inflammatory cytokines during reproductive tract infections, affects the HPG axis to reduce testosterone biosynthesis. OS also increases prolactin secretion from the anterior pituitary and E2 synthesis from
testosterone 8136 E2 synthesis from the testis. These two hormones reduce GnRH secretion from the hypothalamus and testosterone biosynthesis from the testis, respectivelyThus, besides the central control through the HPG axis, the
testosterone 13421 increasing stress hormone (cortisol) levels and activating the immune–inflammatory systemDecreases serum testosterone and LH levels by suppressing androgen synthesis and inducing Leydig cells apoptosis Heat stressBy
testosterone 13693 oxidase activity and disrupting mitochondrial homeostasisDisrupts Sertoli cell functions, decreases testosterone and LH levels Environmental toxicantsBy activating inflammatory mechanisms and cellular deathDecreases
testosterone 13952 hormonal biosynthesis Electromagnetic radiationsBy decreasing total antioxidant capacityDecreases serum testosterone and LH levels Long-term heavy exerciseBy stimulating mitochondrial enzymes including NOX and XODecreases
testosterone 14085 levels Long-term heavy exerciseBy stimulating mitochondrial enzymes including NOX and XODecreases LH, FSH, and testosterone levels ObesityBy increasing leptin levels in human endothelial cells and increasing mitochondrial
testosterone 14531 GnRH High-fat and high-protein foodBy decreasing natural food antioxidants and free radical scavengersDecreases testosterone biosynthesis, LH secretion and androgen profile AlcoholBy stimulating cytochrome P450s enzyme activities
testosterone 14811 body, and reducing antioxidant levelsIncreases Sertoli cells and Leydig cells apoptosis, reduces serum testosterone , LH and FSH levels Marijuana and narcotic drugsBy increasing inflammation and cytochrome p53-induced
testosterone 15015 p53-induced apoptotic cell deathInhibits GnRH release and LH production, inhibits HPG axis, reduces testosterone level, and increases SHBG level SmokingBy decreasing oxygen delivery to the testis and the high metabolic
testosterone 15319 metabolites, weakening of the antioxidant defense systems. Stimulation of NOX enzymesAlters plasma levels of testosterone , prolactin, estradiol, FSH, LH and SHBG by affecting the Leydig and Sertoli cells Anabolic steroidsBy
testosterone 15635 apoptosisDisrupts Leydig cell functions, suppresses HPG axis, reduces LH release and thus testicular testosterone biosynthesisEndogenous sources AgingBy decreasing the activities of antioxidant enzymes, alteration
testosterone 15916 peroxidation of Leydig cells, LH sensitivity by diminishing LH receptors, reduces the rate of steroidogenesis, testosterone biosynthesis and secretion Infections of the reproductive tractBacterial strains that colonize the
testosterone 16252 inflammatory mediators, activation of macrophages, lymphocytes and other immunoreactive cellsReduces serum testosterone levels by disrupting the hormonal axis, increase in LH and FSH levelsExogenous factorsPsychological
testosterone 17077 by directly affecting the action of glucocorticoids on Leydig cells [[11]]. As a result, circulating testosterone levels decrease through suppression of androgen synthesis and induction of apoptosis of Leydig cells
testosterone 17573 (11βHSD-1), NADPH was produced as a cofactor that is used for the biosynthesis of steroidogenic enzymes and testosterone [[58]].Stress adversely affects steroidogenesis, since changes in the autonomic catecholaminergic activities
testosterone 17797 during stress may suppress Leydig cell functions, thus inhibiting steroidogenic enzyme activities and testosterone production [[11]]. Stress-induced elevations of glucocorticoid levels can directly decrease testosterone
testosterone 17902 testosterone production [[11]]. Stress-induced elevations of glucocorticoid levels can directly decrease testosterone levels without altering LH levels [[59]–[61]]. Further, in case of chronic stress, a decrease in LH
testosterone 19702 studies have indicated that testicular heat stress leads to a decline in the circulating levels of testosterone and LH but increases serum cortisol levels [[73], [74]]. Testicular heat stress also leads to Leydig
testosterone 19850 levels [[73], [74]]. Testicular heat stress also leads to Leydig cell apoptosis and a reduction in testosterone biosynthesis in adult rat testes [[75]]. Moreover, increased testicular temperature adversely affects
testosterone 21369 [[90]], enhance the level of circulating cortisol owing to OS induction [[91]] and reduces circulating testosterone levels [[92], [93]]. Increased cortisol decreases LH secretion through crosstalk between the HPG-HPA
testosterone 21576 HPG-HPA axes. Decreased LH concentration fails to stimulate the Leydig cells resulting in decreased testosterone production, whereas decreased FSH affects normal Sertoli cell functions [[94]]. These toxicants also
testosterone 23025 increasing the production of cortisol from adrenal cortex [[104]]. These radiations can also decrease testosterone secretion from Leydig cells by disrupting the male reproductive hormonal axis [[105]]. Electromagnetic
testosterone 23498 hypothalamus [[107]]. Thus, altered GnRH levels influence FSH and LH secretion and negatively affects testosterone synthesis in the testis [[108]].ExerciseContrary to regular exercise that enhances antioxidant defences
testosterone 24006 skeletal muscle [[109]]. Some studies showed that moderate physical activity can increase FSH, LH, and testosterone levels [[110]], which is widely associated with increased energy and muscle strength [[111], [112]].
testosterone 24223 Despite the impact of moderate exercise, data suggest that vigorous exercise may decrease LH, FSH, and testosterone levels as well as semen parameters [[113], [114]]. However, other investigators have reported that testosterone
testosterone 24335 levels as well as semen parameters [[113], [114]]. However, other investigators have reported that testosterone levels remain unaltered following heavy exercise [[115], [116]].ObesityObesity is a complex health disorder
testosterone 25145 gonads due to its receptor isoforms in gonadal tissue [[125]].Though the impact of ghrelin on serum testosterone level is contentious [[126]–[128]], it is reported that ghrelin receptors are present in the testis
testosterone 25297 it is reported that ghrelin receptors are present in the testis and that ghrelin plays a key role in testosterone production, but not directly in spermatogenesis [[126]]. Increased ROS levels appear to cause increased
testosterone 25564 result in obesity and further ROS production.Serum adiponectin level is negatively correlated with both testosterone [[130]] and ROS production [[131]]. Orexin (hypocretin) is known to stimulate testosterone production
testosterone 25655 with both testosterone [[130]] and ROS production [[131]]. Orexin (hypocretin) is known to stimulate testosterone production by enhancing the activities of steroidogenic enzymes in Leydig cells [[132]]. It is also
testosterone 27641 reducing OS and improving basic sperm parameters. This improvement can be established by stimulation of testosterone biosynthesis, FSH and LH secretion, inhibin B and enhancement of androgen profile [[144]]. Investigators
testosterone 27880 mainly selenium, coenzyme Q10 (CoQ10), and N-acetyl-cysteine can affect semen parameters by increasing testosterone and inhibin B [[145]]. However, further research is warranted to determine if there are any appropriate
testosterone 29129 linked with the effects of alcohol consumption [[149]]. Chronic alcohol consumption can reduce serum testosterone , LH, and FSH levels by affecting the interactions between the neural and endocrine systems [[149], [150]].
testosterone 30888 increase in serum concentrations of sex hormone binding globulin (SHBG), a protein which tightly binds testosterone and E2 thus restricting the levels of unbound testosterone [[162], [163]]. Therefore, for opioid users,
testosterone 30947 globulin (SHBG), a protein which tightly binds testosterone and E2 thus restricting the levels of unbound testosterone [[162], [163]]. Therefore, for opioid users, the level of total testosterone and E2 remain subnormal
testosterone 31024 the levels of unbound testosterone [[162], [163]]. Therefore, for opioid users, the level of total testosterone and E2 remain subnormal [[162], [163]]. Consequently, decreased testosterone levels also result in the
testosterone 31101 users, the level of total testosterone and E2 remain subnormal [[162], [163]]. Consequently, decreased testosterone levels also result in the decrease of LH levels. The loss of integrity of the HPG axis via opioid actions
testosterone 31359 clinical hypogonadism [[162], [164]]. The opioid methadone is also reported to significantly reduce testosterone levels by directly affecting steroidogenesis [[158]].Marijuana contains the cannabinoid, delta-9-tetrahydrocannabinol
testosterone 31645 [[164]]. Thus, THC, by imposing adversities upon the HPG axis and causing dose-dependent reduction in testosterone production, impairs spermatogenesis [[164], [165]] at different mitotic and meiotic stages, resulting
testosterone 31943 erectile and ejaculatory dysfunction [[166]].Studies showed that heroin can decrease gonadotropin and testosterone levels by affecting the HPG axis [[158]]. Similarly, cocaine exposure can also disrupt normal gonadal
testosterone 32102 Similarly, cocaine exposure can also disrupt normal gonadal functions and are associated with decreased testosterone production and HPG axis dysregulation [[167]].Non-medical use of drug narcotics, such as hydrocodone
testosterone 33174 systems [[171]–[173]]. Studies have indicated that exposure to smoke can change plasma levels of testosterone , PRL, E2, FSH, LH and SHBG by effects on Leydig and Sertoli cells [[171]–[173]]. Studies have also
testosterone 33810 spermatogenesis by suppressing the HPG axis, thus limiting the release of FSH and LH and in turn decreasing testosterone biosynthesis in the testis [[176], [177]]. Hypogonadism associated with anabolic androgenic steroid
testosterone 34179 to achieve [[164]]. AAS abuse primarily produces Leydig cell alterations which lead to a decrease in testosterone synthesis [[177]]. However, disruption in the end stage of spermatogenesis with a lack of mature spermatozoa
testosterone 34595 proliferation but cellular counts generally remain less than normal, accounting for delayed recovery of testosterone levels and the occasional irreversible effects of AAS [[179]].Endogenous factorsThough endogenous ROS
testosterone 35167 oxidative modifications of DNA and alterations in the mitochondrial membrane potential required for testosterone synthesis take place [[181], [182]]. Alongside these changes, an increase in LH sensitivity due to diminishing
testosterone 36010 [[185], [188], [189]]. Furthermore, following ROS production, the activities of several enzymes of the testosterone biosynthetic pathway are reduced, resulting in further decrease in testosterone synthesis and secretion
testosterone 36090 several enzymes of the testosterone biosynthetic pathway are reduced, resulting in further decrease in testosterone synthesis and secretion [[190], [191]].Reproductive tract infectionsReproductive tract infections is
testosterone 37761 fever; (ii) congestion of seminiferous tubule following interstitial oedema; or (iii) modification of testosterone production. Though studies on male sex hormones and reproductive tract infections are scanty, some investigators
testosterone 37913 hormones and reproductive tract infections are scanty, some investigators observed the reduction of testosterone together with an increase in LH and FSH levels in patients with reproductive tract infections [[196]–[198]].
testosterone 38139 has been reported that in patients with chronic prostatitis, corticosterone level decreases, while testosterone level increases compared to normal controls [[199]]. Whereas in mumps orchitis, increased corticosterone
testosterone 38335 increased corticosterone level decreases both LH and FSH levels which results in reduced production of testosterone from Leydig cells [[200]].Hormonal influence on the oxidative status of male reproductionOS that occurs
testosterone 38741 and fragmentation, and steroidogenic enzyme inhibition [[10]]. Testicular OS causes a reduction in testosterone production, either as a result of the injury to the Leydig cells or to other endocrine structures like
testosterone 39478 correlated with spermatogenesis [[204], [205]].It has been reported that systemic hormones (FSH, LH, testosterone , E2, PRL) may regulate seminal total antioxidant capacity (TAC) [[206], [207]]. A positive relationship
testosterone 39769 gonadotropins or gonadal steroids with TAC have also been shown [[22]]. It is evident that some hormones like testosterone and MLT may act as antioxidants to protect sperm and other testicular cells from damage induced by ROS
testosterone 40111 antioxidants, but the proper mechanism is still unclear [[210]]. Direct and indirect relationships between testosterone and antioxidant levels like selenium and/or CoQ10 and between testosterone and zinc in infertile men,
testosterone 40186 indirect relationships between testosterone and antioxidant levels like selenium and/or CoQ10 and between testosterone and zinc in infertile men, respectively, have been observed [[207], [211]]. CoQ10 can decrease FSH and
testosterone 40383 can decrease FSH and LH levels [[212]]. A negative relationship has been found between serum level of testosterone , E2, fT4 and sperm DNA damage [[213], [214]]. Also, the antioxidant inhibition could affect triiodothyronine
testosterone 40800 production [[216]] and the subsequent sperm DNA damage [[217]]. Although it has been reported that testosterone could produce DNA fragmentation in Sertoli and germ cells by stimulating caspase activities in Sertoli
testosterone 40980 stimulating caspase activities in Sertoli cells [[218]], long-term effects of antioxidants can alter FSH, testosterone , and inhibin B levels [[219]].Mechanism of actionInnumerable exogenous and endogenous factors, as discussed
testosterone 41564 secretion from the anterior pituitary. Decreased LH fails to stimulate Leydig cells to produce enough testosterone . Decreased FSH diminishes the release of androgen-binding protein (ABP) from the Sertoli cells, and
testosterone 41718 of androgen-binding protein (ABP) from the Sertoli cells, and thus, an overall decline in circulating testosterone occurs during severe OS.ROS also affect HPT axis to reduce T3 and T4 secretion. Decreased T3 reduces
testosterone 41900 secretion. Decreased T3 reduces the levels of the StAR mRNA and protein in Leydig cells, as well as testosterone production [[220]]. Increased OS also decreases the secretion of insulin from the pancreas which further
testosterone 42083 insulin from the pancreas which further negatively affects T3 release from the thyroid gland and thereby testosterone biosynthesis.Conditions such as obesity not only involve the HPA and HPT axes, it also includes several
testosterone 42615 from the hypothalamus.Testicular E2 and inhibin are produced intensely during OS, which then inhibit testosterone release. Following ROS exposure, aromatase activity increases which result in more E2 production. ROS
testosterone 43005 production of pro-inflammatory cytokines (TNF-α, IL-1b, and IL-6) which again inhibit both GnRH release and testosterone secretion.Thus, through its actions on an individual hormonal axis and/or by disrupting the cross-talk
testosterone 43183 axis and/or by disrupting the cross-talk among different endocrine systems, ROS can lead to decreased testosterone production as the outcome of endocrine disruption. Decreased testosterone fails to regulate spermatogenesis
testosterone 43257 ROS can lead to decreased testosterone production as the outcome of endocrine disruption. Decreased testosterone fails to regulate spermatogenesis properly to produce enough mature spermatozoa. It also fails to maintain
testosterone 43527 which play crucial roles in sperm maturation. As a prime regulator of male reproductive behaviour, testosterone deficiency may lead to suppressed sexual behaviour among men. Thus, by disrupting the endocrine reproductive
Select Disease Character Offset Disease Term Instance
hypogonadism 5664 modulation of dopaminergic pathway may also reduce LH and testosterone level and thus is associated with hypogonadism [[22]]. Dehydroepiandrosterone (DHEA) is another male reproduction ameliorating, steroid hormone secreted
hypogonadism 31268 loss of integrity of the HPG axis via opioid actions on sex hormones and LH levels, lead to clinical hypogonadism [[162], [164]]. The opioid methadone is also reported to significantly reduce testosterone levels by
obesity 7679 the thyroid gland and through HPT-HPG axes cross-talk decreases testosterone biosynthesis. ROS production in obesity also increases circulating leptin levels which directly reduces testosterone synthesis in the testis.
obesity 25470 Increased ROS levels appear to cause increased levels of ghrelin [[129]] which may, in turn, result in obesity and further ROS production.Serum adiponectin level is negatively correlated with both testosterone [[130]]
obesity 25979 indirectly reduce the androgen profile in men.The complex cross-talk among these hormones is interrupted in obesity , thus causing a massive annihilation of the hormonal milieu, which in turn affects male reproductive
obesity 26200 Although there is a body of evidence highlighting the complexity and the multifactorial effects that obesity has on certain male reproductive functions, the correlation between obesity and semen parameters is
obesity 26276 multifactorial effects that obesity has on certain male reproductive functions, the correlation between obesity and semen parameters is still debated [[134], [135]].Food intakeThere is an inverse relationship between
obesity 42128 affects T3 release from the thyroid gland and thereby testosterone biosynthesis.Conditions such as obesity not only involve the HPA and HPT axes, it also includes several metabolic hormones that manifest ROS-induced

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