Oxidative stress and DNA damage in peripheral blood mononuclear cells from normal, obese, prediabetic and diabetic persons exposed to adrenaline in vitro

Djelić, Ninoslav; Radaković, Milena; Borozan, Sunčica; Dimirijević-Srećković, Vesna; Pajović, Nevena; Vejnović, Branislav; Borozan, Nevena; Bankoglu, Ezgi Eyluel; Stopper, Helga; Stanimirović, Zoran

doi:10.1016/j.mrgentox.2019.01.013

Cited by 15 publications

(6 citation statements)

References 49 publications

(55 reference statements)

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“…Hence, it is not surprising that obesity contributes to the ethiopathogenesis of diabetes complications [ 18 ]. Moreover, results of this investigation are in accordance with our previous finding that PMBCs from obese, prediabetics, and diabetics treated with the stress hormone adrenaline had a higher level of DNA damage in comparison to normal persons [ 19 ].…”

Section: Discussionsupporting

confidence: 91%

Oxidative Stress and DNA Damage in Peripheral Blood Mononuclear Cells from Normal, Obese, Prediabetic and Diabetic Persons Exposed to Thyroid Hormone In Vitro

Djelić

Borozan

Dimitrijević-Srećković

et al. 2022

IJMS

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Diabetes, a chronic group of medical disorders characterized byhyperglycemia, has become a global pandemic. Some hormones may influence the course and outcome of diabetes, especially if they potentiate the formation of reactive oxygen species (ROS). There is a close relationship between thyroid disorders and diabetes. The main objective of this investigation was to find out whether peripheral blood mononuclear cells (PBMCs) are more prone to DNA damage by triiodothyronine (T3) (0.1, 1 and 10 μM) at various stages of progression through diabetes (obese, prediabetics, and type 2 diabetes mellitus—T2DM persons). In addition, some biochemical parameters of oxidative stress (catalase-CAT, thiobarbituric acid reactive substances—TBARS) and lactate dehydrogenase (LDH) were evaluated. PBMCs from prediabetic and diabetic patients exhibited increased sensitivity for T3 regarding elevated level of DNA damage, inhibition of catalase, and increase of TBARS and LDH. PBMCs from obese patients reacted in the same manner, except for DNA damage. The results of this study should contribute to a better understanding of the role of thyroid hormones in the progression of T2DM.

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Section: Discussionsupporting

confidence: 91%

Oxidative Stress and DNA Damage in Peripheral Blood Mononuclear Cells from Normal, Obese, Prediabetic and Diabetic Persons Exposed to Thyroid Hormone In Vitro

Djelić

Borozan

Dimitrijević-Srećković

et al. 2022

IJMS

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“…As expected from these data, when we compared the gene expression under IH with IH and epinephrine together, there were only few genes that were differentially expressed consistent with loss of epinephrine-effect on gene expression. While further studies will be needed to understand the exact mechanisms behind these unexpected findings, we speculate that one possibility that may exert beneficial effects on the cardiovascular system by activating antioxidant pathways 46,47 , which then may provide protection by inhibiting catecholamine-induced oxidative stress [48][49][50] . Contrary to the notion that OSA, which is characterized by IH as its hallmark, is an independent risk factor for cardiovascular disease, several studies have shown that IH conditioning may be cardioprotective both in experimental models as well as humans 51 .…”

Section: Discussionmentioning

confidence: 89%

Intermittent hypoxia inhibits epinephrine-induced transcriptional changes in human aortic endothelial cells

Çetin-Atalay

Meliton

Sun

et al. 2022

Sci Rep

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Obstructive sleep apnea (OSA) is an independent risk factor for cardiovascular disease. While intermittent hypoxia (IH) and catecholamine release play an important role in this increased risk, the mechanisms are incompletely understood. We have recently reported that IH causes endothelial cell (EC) activation, an early phenomenon in the development of cardiovascular disease, via IH-induced catecholamine release. Here, we investigated the effects of IH and epinephrine on gene expression in human aortic ECs using RNA-sequencing. We found a significant overlap between IH and epinephrine-induced differentially expressed genes (DEGs) including enrichment in leukocyte migration, cytokine-cytokine receptor interaction, cell adhesion and angiogenesis. Epinephrine caused higher number of DEGs compared to IH. Interestingly, IH when combined with epinephrine had an inhibitory effect on epinephrine-induced gene expression. Combination of IH and epinephrine induced MT1G (Metallothionein 1G), which has been shown to be highly expressed in ECs from parts of aorta (i.e., aortic arch) where atherosclerosis is more likely to occur. In conclusion, epinephrine has a greater effect than IH on EC gene expression in terms of number of genes and their expression level. IH inhibited the epinephrine-induced transcriptional response. Further investigation of the interaction between IH and epinephrine is needed to better understand how OSA causes cardiovascular disease.

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“…Adrenaline treatment down-regulated the expression of AANAT and MT1 and led to declined melatonin levels in these tissues. In addition to its auto-oxidation mediated indirect blocking of the melatonergic system (9), adrenaline might also directly interact with AANAT and MT1 genes to induce DNA damage (10,12,48). However, pretreatment of melatonin efficiently increased the expressions of AANAT and MT1and enhanced the melatonin levels in stomach, duodenum and colon tissues indicating restoration of endogenous melatonergic system which was impeded by adrenaline.…”

Section: Discussionmentioning

confidence: 99%

Amelioration of adrenaline induced oxidative gastrointestinal damages in rat by melatonin through SIRT1-NFκB and PGC1α-AMPKα cascades

Pal¹,

Sarkar²,

Mishra³

et al. 2020

Melatonin Res.

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Adrenaline at high pharmacological doses may lead to oxidative damages in diverse organs including gut. In this study, we attempt to elucidate the potentially protective effects of melatonin on gastrointestinal (GI) tissue damages induced by adrenaline. Rats were injected (s.c.) with different doses (0.125, 0.25 and 0.50 mg/kg) of adrenaline bitartrate (AD) for 15 days with or without melatonin (2.5, 5 and 10 mg/kg; orally). The results showed that adrenaline caused massive histological and ultra-structural GI injuries and melatonin (20 mg/kg) effectively protected these injuries. The protective mechanisms are related to the antioxidant and anti-inflammatory activities of melatonin indicated by increased glutathione levels and antioxidant enzymes as well as decreased oxidative stress markers and pro-inflammatory cytokines in GI tissues. The signal pathways of melatonin include up-regulating expression of Nrf2, SIRT1 and Bcl2, while down-regulating NFκB, TNFα and Bax. Melatonin also targeted mitochondrial energy homeostasis and biogenesis by up-regulating expression of PGC1α, AMPKα and SOD2 and reduced leakage of cytochrome c. The SIRT1-NFκB and PGC1α-AMPKα signal transduction pathways seem to play the central roles involving in melatonin’s protective effects on gastric damages induced by the high doses of adrenaline.

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Oxidative stress and DNA damage in peripheral blood mononuclear cells from normal, obese, prediabetic and diabetic persons exposed to adrenaline in vitro

Cited by 15 publications

References 49 publications

Oxidative Stress and DNA Damage in Peripheral Blood Mononuclear Cells from Normal, Obese, Prediabetic and Diabetic Persons Exposed to Thyroid Hormone In Vitro

Oxidative Stress and DNA Damage in Peripheral Blood Mononuclear Cells from Normal, Obese, Prediabetic and Diabetic Persons Exposed to Thyroid Hormone In Vitro

Intermittent hypoxia inhibits epinephrine-induced transcriptional changes in human aortic endothelial cells

Amelioration of adrenaline induced oxidative gastrointestinal damages in rat by melatonin through SIRT1-NFκB and PGC1α-AMPKα cascades

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