Euterpe oleracea (Martius) Oil Reverses Testicular Alterations Caused after Cadmium Administration

Mouro, Viviane Gorete Silveira; Melo, Fabiana Cristina Silveira Alves de; Martins, Ana Luiza; Gomes, Marcos de Lucca Moreira; Oliveira, Jerusa Maria de; Freitas, Mariella Bontempo; Demuner, Antônio J.; Leite, João Paulo Viana; Matta, Sérgio Luís Pinto da

doi:10.1007/s12011-019-02004-x

Cited by 9 publications

(5 citation statements)

References 59 publications

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“…Research into the impact of polyphenols on male reproduction is scarce; a study in sheep has shown that under restraint stress, a polyphenol-rich dietary supplement improved semen parameters and the expression of antioxidant enzymes in the testes [ 58 ]. A recent study showed that administration of an oil extract from E. oleracea fruits was able to limit the damaging effects of cadmium toxicity, rescuing germ cell viability, restoring testosterone concentration and significantly increasing superoxide dismutase (SOD) activity in the testis [ 35 ]. These results suggest that acai contains compounds which actively contribute to the restoration of homeostasis in tissues under considerable oxidative challenge.…”

Section: Discussionmentioning

confidence: 99%

“…Consumption of acai has been shown to decrease plasma oxidant capacity [ 31 ], serum oxLDL and malondialdehyde [ 32 ] in humans, indicating potential alleviation of oxidative stress in vivo. In rodent models, treatment with acai has significantly reduced tissue levels of malondialdehyde [ 33 ] and proteins with oxidative modifications [ 34 ], improved germ cell viability and testicular antioxidant enzyme activity following cadmium toxicity [ 35 ], and was able to prevent DNA damage in peripheral blood cells in response to a genotoxic agent [ 36 ]. These studies suggest that acai could potentially reduce both oxidative stress and DNA damage in vivo.…”

Section: Introductionmentioning

confidence: 99%

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Mitigating the Effects of Oxidative Sperm DNA Damage

et al. 2020

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Sperm DNA damage is correlated with reduced embryo development and increased miscarriage risk, reducing successful conception. Given its links with oxidative stress, antioxidants have been investigated as a potential treatment, yet results are conflicting. Importantly, individual antioxidants are not identical in composition, and some compounds may be more effective than others. We investigated the use of the polyphenol-rich, high-antioxidant-capacity fruit acai as a treatment for elevated sperm DNA fragmentation (>16%), measured by terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL). Following ≥ 74 days of treatment, we observed a significant decrease in sperm DNA fragmentation (−17.0% ± 2.5%) to 11.9 ± 1.7% (0–37%), with a 68.6% success rate (defined as post-treatment TUNEL < 16%). Post-treatment decreases in DNA fragmentation and success rates were not significantly impacted by low motility and/or concentration, or exceptionally high (> 25%) TUNEL. Treatment significantly reduced concentration in men with normal semen parameters, but 88% remained normal. Overall, successful treatment was not associated with age, semen parameters or TUNEL result at baseline. However, body mass index was significantly higher in nonresponders at baseline. This study provides evidence of a low-cost, effective treatment for elevated sperm DNA damage using acai.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mitigating the Effects of Oxidative Sperm DNA Damage

et al. 2020

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“…In addition, an increased level of TNF-α along with a decreased number of proliferating cell nuclear antigens (PCNA) was detected [ 192 ]. In another study, rats receiving a daily dose of 4.28 mg/kg CdCl 2 (2.62 mg/kg Cd/day) for 7 days showed damage in the epithelium of seminiferous tubules, decreased concentration of serum testosterone and SOD activity [ 193 ]. Similarly, when rats were given a single oral supplementation of 10 mg/kg body weight of CdCl 2 , a significant decrease in the level of serum testosterone and increased lipid peroxidation (MDA) were noted.…”

Section: Environmental Factorsmentioning

confidence: 99%

“…Endothelial NOS expression increases in germ cells exposed to Cd along with higher apoptotic indices that showed the inhibitory effect of NO on spermatogenesis. Apart from increased NO, reduced activity of SOD, catalase, and consequent oxidative stress may damage testicular tissues [ 193 ]. Cd 2+ structurally resemble Ca 2+ [ 197 ] in the cell membrane that may change the integrity of the membrane of sperm acrosome, which can lead to abnormal acrosomal reaction and hamper fertility.…”

Section: Environmental Factorsmentioning

confidence: 99%

Environmental Factors-Induced Oxidative Stress: Hormonal and Molecular Pathway Disruptions in Hypogonadism and Erectile Dysfunction

et al. 2021

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Hypogonadism is an endocrine disorder characterized by inadequate serum testosterone production by the Leydig cells of the testis. It is triggered by alterations in the hypothalamic–pituitary–gonadal axis. Erectile dysfunction (ED) is another common disorder in men that involves an alteration in erectile response–organic, relational, or psychological. The incidence of hypogonadism and ED is common in men aged over 40 years. Hypogonadism (including late-onset hypogonadism) and ED may be linked to several environmental factors-induced oxidative stresses. The factors mainly include exposure to pesticides, radiation, air pollution, heavy metals and other endocrine-disrupting chemicals. These environmental risk factors may induce oxidative stress and lead to hormonal dysfunctions. To better understand the subject, the study used many keywords, including “hypogonadism”, “late-onset hypogonadism”, “testosterone”, “erectile dysfunction”, “reactive oxygen species”, “oxidative stress”, and “environmental pollution” in major online databases, such as SCOPUS and PUBMED to extract relevant scientific information. Based on these parameters, this review summarizes a comprehensive insight into the important environmental issues that may have a direct or indirect association with hypogonadism and ED in men. The study concludes that environmental factors-induced oxidative stress may cause infertility in men. The hypothesis and outcomes were reviewed critically, and the mechanistic approaches are applied through oxidant-sensitive pathways. This study also provides reccomendations on future therapeutic interventions and protective measures against such adverse environmental factors-induced hypogonadism and ED.

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“…Testes are especially vulnerable to Cd exposure. At the tissue level it may result in endothelial damage, hemorrhage, edema and testis calcification (Marettová et al, 2010;Mouro et al, 2020). At the molecular level Cd is known for its disruption of redox balance and specific disintegration of blood-testis barrier (BTB) and Sertoli cell-spermatid adhesion (Chen et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Selenoproteins and their emerging roles in signaling pathways

Stanishevska

2020

Regul. Mech. Biosyst.

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The functional activity of selenoproteins has a wide range of effects on complex pathogenetic processes, including teratogenesis, immuno-inflammatory, neurodegenerative. Being active participants and promoters of many signaling pathways, selenoproteins support the lively interest of a wide scientific community. This review is devoted to the analysis of recent data describing the participation of selenoproteins in various molecular interactions mediating important signaling pathways. Data processing was carried out by the method of complex analysis. For convenience, all selenoproteins were divided into groups depending on their location and function. Among the group of selenoproteins of the ER membrane, selenoprotein N affects the absorption of Ca2+ by the endoplasmic reticulum mediated by oxidoreductin (ERO1), a key player in the CHOP/ERO1 branch, a pathogenic mechanism that causes myopathy. Another selenoprotein of the ER membrane selenoprotein K binding to the DHHC6 protein affects the IP3R receptor that regulates Ca2+ flux. Selenoprotein K is able to affect another protein of the endoplasmic reticulum CHERP, also appearing in Ca2+ transport. Selenoprotein S, associated with the lumen of ER, is able to influence the VCP protein, which ensures the incorporation of selenoprotein K into the ER membrane. Selenoprotein M, as an ER lumen protein, affects the phosphorylation of STAT3 by leptin, which confirms that Sel M is a positive regulator of leptin signaling. Selenoprotein S also related to luminal selenoproteins ER is a modulator of the IRE1α-sXBP1 signaling pathway. Nuclear selenoprotein H will directly affect the suppressor of malignant tumours, p53 protein, the activation of which increases with Sel H deficiency. The same selenoprotein is involved in redox regulation. Among the cytoplasmic selenoproteins, abundant investigations are devoted to SelP, which affects the PI3K/Akt/Erk signaling pathway during ischemia/reperfusion, is transported into the myoblasts through the plasmalemma after binding to the apoER2 receptor, and into the neurons to the megaline receptor and in general, selenoprotein P plays the role of a pool that stores the necessary trace element and releases it, if necessary, for vital selenoproteins. The thioredoxin reductase family plays a key role in the invasion and metastasis of salivary adenoid cystic carcinoma through the influence on the TGF-β-Akt/GSK-3β pathway during epithelial-mesenchymal transition. The deletion of thioredoxin reductase 1 affects the levels of messengers of the Wnt/β-catenin signaling pathway. No less studied is the glutathione peroxidase group, of which GPX3 is able to inhibit signaling in the Wnt/β-catenin pathway and thereby inhibit thyroid metastasis, as well as suppress protein levels in the PI3K/Akt/c-fos pathway. A key observation is that in cases of carcinogenesis, a decrease in GPX3 and its hypermethylation are almost always found. Among deiodinases, deiodinase 3 acts as a promoter of the oncogenes BRAF, MEK or p38, while stimulating a decrease in the expression of cyclin D1. The dependence of the level of deiodinase 3 on the Hedgehog (SHH) signaling pathway is also noted. Methionine sulfoxide reductase A can compete for the uptake of ubiquitin, reduce p38, JNK and ERK promoters of the MAPK signaling pathway; methionine sulfoxide reductase B1 suppresses MAPK signaling messengers, and also increases PARP and caspase 3.

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Euterpe oleracea (Martius) Oil Reverses Testicular Alterations Caused after Cadmium Administration

Cited by 9 publications

References 59 publications

Mitigating the Effects of Oxidative Sperm DNA Damage

Mitigating the Effects of Oxidative Sperm DNA Damage

Environmental Factors-Induced Oxidative Stress: Hormonal and Molecular Pathway Disruptions in Hypogonadism and Erectile Dysfunction

Selenoproteins and their emerging roles in signaling pathways

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