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Helena Martynowicz

Publications and source records attributed to Helena Martynowicz.

5 recordsLinked to original sources
PubMed2025

The importance of dopamine levels and single-nucleotide polymorphism within COMT, DRD1 and DRD2 genes in obstructive sleep apnoea.

BACKGROUND: Obstructive sleep apnoea (OSA) is a prevalent sleep disorder that contributes to serious cardiovascular comorbidities. While the mechanical aspects of OSA are well-studied, its neurobiological underpinnings remain underexplored. In this study, we investigated the role of dopamine and its genetic modulators in OSA pathophysiology. PATIENTS AND METHODS: Serum dopamine levels were assessed in a cohort of 153 participants (96 OSA patients and 57 controls), and single-nucleotide polymorphisms (SNPs) in dopamine-related genes, including COMT, DRD1 and DRD2, were analysed in a cohort of 286 participants (141 OSA patients and 145 controls). RESULTS: Elevated serum dopamine levels were observed in OSA patients (p = 0.01), with dopamine levels correlating independently with OSA and male gender. Genotypic analysis identified the DRD2 rs1800497 T allele as a potential independent predictor of OSA severity (p = 0.011), hypopnea (p = 0.005) and arousals (p = 0.024). CONCLUSIONS: This study advances the understanding of OSA by identifying elevated dopamine levels and genetic variations in DRD2 rs1800497 as potential modulators of its occurrence and severity. These findings pave the way for personalized diagnostic and therapeutic approaches. By integrating neurobiology, genetics, and clinical practice, this research contributes to the evolving framework for precision medicine in sleep disorders.

Humans↗
PubMed2005

[Occupational risk factors and male breast cancer].

Male breast cancer is rare compared to its female counterpart and makes less than 1% of all breast cancer. Its etiology is less known than that of female breast cancer. Numerous experimental and clinical studies indicate the possibility of an increased risk of male breast cancer in workers occupationally exposed to electromagnetic field, light at night, and high temperature. There are also studies, which reveal the increased risk of this disease induced by occupational exposure to pesticides, aromatic hydrocarbons and ionizing radiation. However, irrefutable epidemiologic data from prospective clinical trials have not yet been obtained.

Breast Neoplasms, Male↗
PubMed2005

[The influence of lead on testis function].

The deterioration of male fertility, found in numerous epidemiological studies of past decades, can be connected to growing exposure to environmental toxins. Heavy metals, especially lead is widely spread and extremely toxic. The mechanism by which lead exerts toxic effects on testis is quite complex. It involves spermatogenesis, steroidogenesis, and red-ox system. The chronic lead exposure can induce functional disorder (decrease of testosterone synthesis) or morphological disorder (decrease of testicular weight and seminal vesicle, peritubular fibrosis, seminiferous tubular diameter decrease and decrease in germ cell population related to an apoptotic process). Currently existing environmental and occupational exposure to lead and increasing combined exposure to environmental toxins results in constantly increasing number of diagnosed fertility impairments.

Causality↗
PubMed2004

Serum vasoactive agents in rats poisoned with cadmium.

OBJECTIVES: Mechanisms of the vascular effect of cadmium vary and involve nervous, hormone and intracellular signaling pathways. However, it is still not clear if mechanisms of the vascular effect of cadmium (Cd) include changes in the synthesis or release of vasoactive agents. The aim of this study was to evaluate the impact of subchronic Cd poisoning on blood nitric oxide or endothelin in blood and to relate it to the redox system activity in vessel walls and to blood Cd concentration. MATERIALS AND METHODS: The study was performed on male Buffalo rats which were given cadmium in drinking water, 50 or 200 ppm, for 12 weeks. RESULTS: The study showed different dose-dependent changes in toxicological and biochemical status. Mean serum nitric oxide concentration (measured using R&D Systems) was lower in rats poisoned with cadmium compared with the control group (57.7 +/- 7.6 vs. control 65.0 +/- 4.9 micromol/l, p < 0.05), whereas the plasma endothelin-1 level (measured using enzymoimmunoassay) and serum prostaglandin PGF2alpha concentration (determined using R&D System) were similar in all animals. The lipid peroxides concentration (measured colorimetrically) was higher in the group treated with cadmium in a dose of 50 ppm than in controls (5.2 +/- 3.0 vs. controls 1.4 +/- 0.4 nmol/ml, p < 0.001) and gluthatione concentration was decreased in the group treated with cadmium in a dose of 200 ppm as compared with the control group, (1.3 +/- 1.2 vs. control 2.5 +/- 0.9, micromol/l p < 0.05). CONCLUSIONS: It is concluded, that cadmium induces oxidative stress in both doses, however, the activity of defending mechanisms depends on Cd dose. Oxidative stress can be responsible for decreased nitric oxide concentration in serum. We suppose that the mechanisms of the vascular effect of cadmium vary and are dose-dependent. Cd used in a dose of 50 ppm for three months induces more severe functional vascular disturbances than its dose of 200 ppm.

Analysis of Variance↗