Study of GT-repeat expansion in Heme oxygenase-1 gene promoter as genetic cause of male infertility

Siasi, Elham; Aleyasin, Ahmad; Mowla, Seyed Javad; Sahebkashaf, H.

doi:10.1007/s10815-011-9574-0

Cited by 7 publications

(6 citation statements)

References 26 publications

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“…With respect to their (GT)n genotype, liver samples were divided into two classes -those containing short alleles (less than 25 repeats; class S) and those containing long alleles (greater than or equal to 25 repeats; class L). Haplotype analyses confirmed the dominance of the A (-413)T SNP over (GT)n polymorphism [16] . The results of transient transfection assays using luciferase promoter constructs were consistent with in vitro assays carried out in lymphoblastoid cell lines containing HO-1 GT repeats of various lengths [9] .…”

Section: Polymorphismsmentioning

confidence: 67%

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Origassa¹,

Câmara²

2013

WJH

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The activation of heme oxygenase-1 (HO-1) appears to be an endogenous defensive mechanism used by cells to reduce inflammation and tissue damage in a number of injury models. HO-1, a stress-responsive enzyme that catabolizes heme into carbon monoxide (CO), biliverdin and iron, has previously been shown to protect grafts from ischemia/reperfusion and rejection. In addition, the products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin, have been shown to exert protective effects in the liver against a number of stimuli, as in chronic hepatitis C and in transplanted liver grafts. Furthermore, the induction of HO-1 expression can protect the liver against damage caused by a number of chemical compounds. More specifically, the CO derived from HO-1-mediated heme catabolism has been shown to be involved in the regulation of inflammation; furthermore, administration of REVIEW 541October 27, 2013|Volume 5|Issue 10| WJH|www.wjgnet.com low concentrations of exogenous CO has a protective effect against inflammation. Both murine and human HO-1 deficiencies have systemic manifestations associated with iron metabolism, such as hepatic overload (with signs of a chronic hepatitis) and iron deficiency anemia (with paradoxical increased levels of ferritin). Hypoxia induces HO-1 expression in multiple rodent, bovine and monkey cell lines, but interestingly, hypoxia represses expression of the human HO-1 gene in a variety of human cell types (endothelial cells, epithelial cells, T cells). These data suggest that HO-1 and CO are promising novel therapeutic molecules for patients with inflammatory diseases. In this review, we present what is currently known regarding the role of HO-1 in liver injuries and in particular, we focus on the implications of targeted induction of HO-1 as a potential therapeutic strategy to protect the liver against chemically induced injury.

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Section: Polymorphismsmentioning

confidence: 67%

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Origassa¹,

Câmara²

2013

WJH

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“…49 The GT-repeat polymorphic region in the promoter of human Heme oxygenase-1 (HO-1) allows this gene to alter its expression level in response to oxidative stress; decreased HO-1 protein levels in seminal plasma in oligospermia or azoospermia patients suggest a low response capacity to ROS stimulation. 54 As i III -induced oxidative stress has been linked to male infertility in animals; 30−32 rats and mice exposed to As i III exhibit a decrease in weight of their testes, epididymis, prostate gland, and seminal vesicles, along with low semen quality including decreases in sperm count, normal morphology, motility, and viability. 30−32 Testicular antioxidant enzyme activities including SOD, catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and glutathione reductase (GR) were also decreased following As i III treatment.…”

Section: Environmental Science and Technologymentioning

confidence: 99%

Urinary Metabolic Biomarkers Link Oxidative Stress Indicators Associated with General Arsenic Exposure to Male Infertility In a Han Chinese Population

Shen¹,

Wang²,

Zhang³

et al. 2013

Environ. Sci. Technol.

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To investigate the hypothesis that general environmental arsenic (As) exposure can impair male fertility, we designed a case-control study examining possible correlations between the concentrations of different As species in urine [controls (n = 151) vs cases (n = 140)], urinary metabolic biomarkers [controls (n = 158) vs cases (n = 135)], and infertility characterized by poor semen quality. Regional participants were recruited sequentially from the affiliated hospitals of Nanjing Medical University. Elevated inorganic arsenate (Asi(V)) exposure was associated with infertility: in comparison with the first quartile, subjects with Asi(V) levels above the median were more likely to exhibit male idiopathic infertility with increasing adjusted odds ratios (AOR) of 4.9 [95% confidence interval (CI), 1.8-13.6] and 13.6 (95% CI, 4.8-38.6) at the third and fourth quartiles (P = 0.000 for trend), respectively. Other As species did not exhibit a significant dose-dependent correlation with infertility risk. Levels of urinary biomarkers correlated with both male infertility and Asi(V) concentrations [controls (n = 145) vs cases (n = 123)]; the latter correlation was independent of disease. These included acylcarnitines, aspartic acid, and hydroxyestrone, which were negatively associated with infertility, and uridine and methylxanthine, which were positively associated. In conclusion, for the first time we show that elevated urinary concentrations of Asi(V) from general As exposure are significantly associated with male infertility, and As species may exert toxicity via oxidative stress and sexual hormone disrupting mechanisms, as indicated by related biomarkers.

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“…Thus, HO-1 deficiency is associated with a low birth rate in mice, and microsatellite polymorphisms on the promoter of HO-1, associated with lower expression, were involved in preeclampsia in humans [126,127]. Although the role of HO-1 in the male reproductive tract is less understood, HO-1 polymorphisms, linked to low levels of expression, are related to male infertility, supporting an HO-1 positive effect on spermatogenesis [128]. If HO-1 role is linked to its pro-survival, antioxidant, or anti-inflammatory effects is not fully established in this case.…”

Section: Ho-1 Role In the Reproductive Tractmentioning

confidence: 99%

Heme Oxygenase 1 in Vertebrates: Friend and Foe

Silva

Correa

2021

Cell Biochem Biophys

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HO-1 is the inducible form of the enzyme heme-oxygenase. HO-1 catalyzes heme breakdown, reducing the levels of this important oxidant molecule and generating antioxidant, anti-inflammatory, and anti-apoptotic byproducts. Thus, HO-1 has been described as an important stress response mechanism during both physiologic and pathological processes. Interestingly, some findings are demonstrating that uncontrolled levels of HO-1 byproducts can be associated with cell death and tissue destruction as well. Furthermore, HO-1 can be located in the nucleus, influencing gene transcription, cellular proliferation, and DNA repair. Here, we will discuss several studies that approach HO-1 effects as a protective or detrimental mechanism in different pathological conditions. In this sense, as the major organs of vertebrates will deal specifically with distinct types of stresses, we discuss the HO-1 role in each of them, exposing the contradictions associated with HO-1 expression after different insults and circumstances.

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Study of GT-repeat expansion in Heme oxygenase-1 gene promoter as genetic cause of male infertility

Cited by 7 publications

References 26 publications

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Urinary Metabolic Biomarkers Link Oxidative Stress Indicators Associated with General Arsenic Exposure to Male Infertility In a Han Chinese Population

Heme Oxygenase 1 in Vertebrates: Friend and Foe

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