A Role for Bromine Deficiency in Sleep Disturbances of Long-Term Dialysis Patients

Canavese, Caterina; Costanzi, Ester De; Stratta, Piero; Sabbioni, E.

doi:10.1053/j.ajkd.2006.08.033

Cited by 9 publications

(5 citation statements)

References 8 publications

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“…Long‐term administration of fibrates impairs liver function and causes muscle damage . Notably, as an essential trace element, bromide plays a pivotal role in maintaining redox homeostasis at a serum concentration of 42 ~ 61 μM in healthy individuals . Therefore, the doses we selected were in a tolerable range to humans and were much lower than those used in the clinic (~2.1 mM).…”

Section: Discussionmentioning

confidence: 80%

Bromide alleviates fatty acid‐induced lipid accumulation in mouse primary hepatocytes through the activation of PPARα signals

Shi

Zhang

Cheng

et al. 2019

J Cellular Molecular Medi

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Increased plasma free fatty acids (FFAs) and liver triglyceride (TG) accumulations have been implicated in the pathogenesis of hepatic steatosis. On the other hand, trace elements function as essential cofactors that are involved in various biochemical processes in mammals, including metabolic homeostasis. Notably, clinical and animal studies suggest that the plasma levels of bromide negatively correlate with those of TG, total cholesterol (TC) and high‐density lipoprotein‐cholesterol (HDL‐C). However, the effect of bromide on lipid accumulation and the direct molecular target responsible for its action remains unknown. Oil red O (ORO) and Nile red staining were used to detect the effect of bromide on lipid accumulation in mouse primary hepatocytes (PHs) treated with different doses of sodium bromide (NaBr) in the presence of FFAs (0.4 mM oleate/palmitic acid 1:1). Spectrophotometric and fluorometric analyses were performed to assess cellular TG concentrations and rates of fatty acid oxidation (FAO), respectively, in mouse PHs. We found that bromide decreased FFA‐induced lipid accumulation and increased FFA‐inhibited oxygen consumptions in mouse PHs in a dose‐dependent manner via activation of PPARα . Mechanical studies demonstrated that bromide decreased the phosphorylation levels of JNK. More importantly, the PPARα ‐specific inhibitor GW6471 partially abolished the beneficial effects of bromide on mouse PHs. Bromide alleviates FFA‐induced excessive lipid storage and increases rates of FAO through the activation of PPARα /JNK signals in mouse PHs. Therefore, bromide may serve as a novel drug in the treatment of hepatic steatosis.

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Section: Discussionmentioning

confidence: 80%

Bromide alleviates fatty acid‐induced lipid accumulation in mouse primary hepatocytes through the activation of PPARα signals

Shi

Zhang

Cheng

et al. 2019

J Cellular Molecular Medi

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“…Interestingly, the possible association between bromine deficiency and insomnia in hemodialysis patients was suggested more than 40 years ago, but later seems to have been forgotten [ 54 ]. Many years later (in 2006), Canavese et al [ 55 ] raised the question again, noting that bromine is associated with brain metabolism, is used as a sedative to induce sleep, and increases in animals during hibernation as well as in sleeping humans, further highlighting the discovery of a bromine compound with REM-sleep-inducing and anti-cholinesterase activities that was isolated from human cerebrospinal fluid and identified as 1-methylheptyl gamma-bromoacetoacetate The authors concluded with a strong suggestion “that further studies address the evaluation of bromine status in dialysis patients”, which was what we intended in this study. Future studies should address another recommendation by Canavese et al, that of assessing whether supplementation, when indicated, may contribute to the correction of sleep disturbances that affect patients on hemodialysis [ 55 ].…”

Section: Discussionmentioning

confidence: 99%

Serum Iodine and Bromine in Chronic Hemodialysis Patients—An Observational Study in a Cohort of Portuguese Patients

Novakova

Bonev

Duro

et al. 2023

Toxics

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Background: Patients on chronic hemodialysis therapy are at high risk of disturbances in trace element status due to both the underlying disease and the hemodialysis process itself. Data on iodine and bromine levels in these patients are scarce. Methods: Using an ICP-MS analytical procedure, serum iodine and bromine levels were determined in a cohort (n = 57) of end-stage renal disease patients on chronic hemodialysis. The results were compared with those of a control group (n = 59). Results: Hemodialysis patients presented serum iodine levels within the normal range, slightly lower than in controls, but without reaching a statistically significant difference (67.6 ± 17.1 µg/L vs. 72.2 ± 14.8 µg/L; p = 0.1252). In contrast, serum bromine levels were much lower in patients (1086 ± 244 µg/L vs. 4137 ± 770 µg/L; p < 0.0001), at values only about 26% of the values observed in controls. Conclusions: Hemodialysis patients had normal serum iodine levels, but highly decreased serum bromine levels. The clinical significance of this finding requires further investigation, but it may be associated with sleep disturbances and fatigue that affect hemodialysis patients.

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“…As an essential trace element, bromide maintains the redox homeostasis at a serum concentration of 426 1 μM in healthy individuals [17,18]. Clinically, high dose bromide (~2.1 mM) is used to treat the epilepsy.…”

Section: Discussionmentioning

confidence: 99%

Bromide impairs the circadian clock and glycolytic homeostasis via disruption of autophagy in rat H9C2 cardiomyocytes

Jiang

et al. 2020

BMC Mol and Cell Biol

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Background: Trace elements function as essential cofactors that are involved in various biochemical processes in mammals. Autophagy is vital for nutrient supplement, which is an important Zeitegber for the circadian homeostasis in heart. Here, we considered the possibility that autophagy, as well as the cardiomyocyte clock and glycolysis are interlinked. Detrimental effects were observed when cardiac system is exposed to bromine containing drugs. This study investigated the effects and mechanisms of bromide on the circadian clock and glycolytic metabolism of H9C2 cardiomyocytes. Results: In the present study, bromide does not affect cell viability and apoptosis of H9C2 cardiomyocytes. Bromide dampens the clock and glycolytic (Hk2 and Pkm2) gene expression rhythmicity in a dose-dependent manner. Additionally, bromide inhibits autophagic process in H9C2 cardiomyocytes. In contrast, rapamycin (an autophagy inducer) dramatically restores the inhibitory effect of NaBr on the mRNA expression levels of clock genes (Bmal1, Cry1 and Rorα) and glycolytic genes (Hk2 and Pkm2). Conclusions: Our results reveal that bromide represses the clock and glycolytic gene expression patterns, partially through inhibition of autophagy.

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A Role for Bromine Deficiency in Sleep Disturbances of Long-Term Dialysis Patients

Cited by 9 publications

References 8 publications

Bromide alleviates fatty acid‐induced lipid accumulation in mouse primary hepatocytes through the activation of PPARα signals

Bromide alleviates fatty acid‐induced lipid accumulation in mouse primary hepatocytes through the activation of PPARα signals

Serum Iodine and Bromine in Chronic Hemodialysis Patients—An Observational Study in a Cohort of Portuguese Patients

Bromide impairs the circadian clock and glycolytic homeostasis via disruption of autophagy in rat H9C2 cardiomyocytes

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