New insight in beryllium toxicity excluding exposure to beryllium-containing dust: accumulation patterns, target organs, and elimination

Drobyshev, Evgenii; Kybarskaya, Larisa; Dagaev, Sergey; Solovyev, Nikolay

doi:10.1007/s00204-019-02432-7

Cited by 16 publications

(2 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This was associated with a fall in hepatic reduced glutathione content and an increase in lipid peroxidation, interpreted as signs of oxidative stress. Overall, little scientific and clinical interest in Be intoxication and liver injury existed, providing insufficient insight on molecular aspects of Be liver injury [ 30 , 31 , 32 , 33 , 34 ]. Issues of Be were also not discussed in a recent excellent and comprehensive review article focusing on many HMs [ 9 ].…”

Section: Berylliummentioning

confidence: 99%

Aluminum, Arsenic, Beryllium, Cadmium, Chromium, Cobalt, Copper, Iron, Lead, Mercury, Molybdenum, Nickel, Platinum, Thallium, Titanium, Vanadium, and Zinc: Molecular Aspects in Experimental Liver Injury

Teschke

2022

IJMS

View full text Add to dashboard Cite

Experimental liver injury with hepatocelluar necrosis and abnormal liver tests is caused by exposure to heavy metals (HMs) like aluminum, arsenic, beryllium, cadmium, chromium, cobalt, copper, iron, lead, mercury, molybdenum, nickel, platinum, thallium, titanium, vanadium, and zinc. As pollutants, HMs disturb the ecosystem, and as these substances are toxic, they may affect the health of humans and animals. HMs are not biodegradable and may be deposited preferentially in the liver. The use of animal models can help identify molecular and mechanistic steps leading to the injury. HMs commonly initiate hepatocellular overproduction of ROS (reactive oxygen species) due to oxidative stress, resulting in covalent binding of radicals to macromolecular proteins or lipids existing in membranes of subcellular organelles. Liver injury is facilitated by iron via the Fenton reaction, providing ROS, and is triggered if protective antioxidant systems are exhausted. Ferroptosis syn pyroptosis was recently introduced as mechanistic concept in explanations of nickel (Ni) liver injury. NiCl2 causes increased iron deposition in the liver, upregulation of cyclooxygenase 2 (COX-2) protein and mRNA expression levels, downregulation of glutathione eroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1), nuclear receptor coactivator 4 (NCOA4) protein, and mRNA expression levels. Nickel may cause hepatic injury through mitochondrial damage and ferroptosis, defined as mechanism of iron-dependent cell death, similar to glutamate-induced excitotoxicity but likely distinct from apoptosis, necrosis, and autophagy. Under discussion were additional mechanistic concepts of hepatocellular uptake and biliary excretion of mercury in exposed animals. For instance, the organic anion transporter 3 (Oat3) and the multidrug resistance-associated protein 2 (Mrp2) were involved in the hepatic handling of mercury. Mercury treatment modified the expression of Mrp2 and Oat3 as assessed by immunoblotting, partially explaining its impaired biliary excretion. Concomitantly, a decrease in Oat3 abundance in the hepatocyte plasma membranes was observed that limits the hepatic uptake of mercury ions. Most importantly and shown for the first time in liver injury caused by HMs, titanium changed the diversity of gut microbiota and modified their metabolic functions, leading to increased generation of lipopolysaccharides (LPS). As endotoxins, LPS may trigger and perpetuate the liver injury at the level of gut-liver. In sum, mechanistic and molecular steps of experimental liver injury due to HM administration are complex, with ROS as the key promotional compound. However, additional concepts such as iron used in the Fenton reaction, ferroptosis, modification of transporter systems, and endotoxins derived from diversity of intestinal bacteria at the gut-liver level merit further consideration.

show abstract

Section: Berylliummentioning

confidence: 99%

Aluminum, Arsenic, Beryllium, Cadmium, Chromium, Cobalt, Copper, Iron, Lead, Mercury, Molybdenum, Nickel, Platinum, Thallium, Titanium, Vanadium, and Zinc: Molecular Aspects in Experimental Liver Injury

Teschke

2022

IJMS

View full text Add to dashboard Cite

show abstract

“…An important feature of beryllium toxicity is a considerable latency period, usually lasting up to 6-10 years. Because most of the attention related to beryllium has been devoted to occupational exposure, the mechanisms of beryllium toxicity are not yet clear [10][11][12].…”

Section: Toxicity Of Berylliummentioning

confidence: 99%

REMOVAL OF BERYLLIUM (Be2+) FROM WATER SAMPLES BY SORPTION PROCESS: A REVIEW

Arar

2021

WPT STN

View full text Add to dashboard Cite

Beryllium (Be2+) is an important industrial metal because of its unusual material properties: it is lighter than aluminium and six times stronger than steel. Beryllium is a strategic metal due to its low density combined with its strength, low neutron absorption, high melting point and high modulus of elasticity. Beryllium is often alloyed with other metals such as copper and is an important component of materials used in the aerospace, automotive, energy, defense, medical, and electronics industries. However, beryllium and its compounds are very toxic, especially to the lungs, skin, and eyes. Beryllium compounds are known carcinogens based on sufficient evidence of carcinogenicity in humans from human studies. Toxic effects of beryllium include immunotoxic, allergic, mutagenic, and carcinogenic effects. Mammalian tissues do not excrete it, so the effects are cumulative and can lead to death at high concentrations. Therefore, removal of Be2+ is important. In this review, the removal of Be2+ from water samples by sorption processes using different sorbents was summarized. The effects of process parameters on the removal of Be2+ have been summarized. The work discussed showed that ion exchange resins, various modified biosorbents metal oxides can be used for the removal of Be2+. The results showed that the pH of the solution has an important effect on the removal rate. Sorption kinetics vary from 3 minutes to 48h. When the functional groups are on the surface of the sorbent, the sorption process is rapid. However, if the surface of the sorbent is covered with oxides such as magnetite, it takes longer to reach equilibrium. Published work shows that more than 99 % of Be2+ can be removed from solution.

show abstract

Hydrogen sulfide alleviates apoptosis and autophagy induced by beryllium sulfate in 16HBE cells

Liu

Yuan

et al. 2021

J of Applied Toxicology

View full text Add to dashboard Cite

Beryllium and its compounds are systemic toxicants that are widely applied in many industries. Hydrogen sulfide has been found to protect cells. The present study aimed to determine the protective mechanisms involved in hydrogen sulfide treatment of 16HBE cells following beryllium sulfate-induced injury. 16HBE cells were treated with beryllium sulfate doses ranging between 0 and 300 μM BeSO 4 .Additionally, 16HBE cells were subjected to pretreatment with either a 300 μM dose of sodium hydrosulfide (a hydrogen sulfide donor) or 10 mM DLpropargylglycine (a cystathionine-γ-lyase inhibitor) for 6 hr before then being treated with 150 μM beryllium sulfate for 48 hr. This study illustrates that beryllium sulfate induces a reduction in cell viability, increases lactate dehydrogenase (LDH) release, and increases cellular apoptosis and autophagy in 16HBE cells.Interestingly, pretreating 16HBE cells with sodium hydrosulfide significantly reduced the beryllium sulfate-induced apoptosis and autophagy. Moreover, it increased the mitochondrial membrane potential and alleviated the G2/M-phase cell cycle arrest. However, pretreatment with 10 mM DL-propargylglycine promoted the opposite effects. PI3K/Akt/mTOR and Nrf2/ARE signaling pathways are also activated following pretreatment with sodium hydrosulfide. These results indicate the protection provided by hydrogen sulfide in 16HBE cells against beryllium sulfate-induced injury is associated with the inhibition of apoptosis and autophagy through the activation of the PI3K/Akt/mTOR and Nrf2/ARE signaling pathways. Therefore, hydrogen sulfide has the potential to be a promising candidate in the treatment against beryllium disease.

show abstract

New insight in beryllium toxicity excluding exposure to beryllium-containing dust: accumulation patterns, target organs, and elimination

Cited by 16 publications

References 41 publications

Aluminum, Arsenic, Beryllium, Cadmium, Chromium, Cobalt, Copper, Iron, Lead, Mercury, Molybdenum, Nickel, Platinum, Thallium, Titanium, Vanadium, and Zinc: Molecular Aspects in Experimental Liver Injury

Aluminum, Arsenic, Beryllium, Cadmium, Chromium, Cobalt, Copper, Iron, Lead, Mercury, Molybdenum, Nickel, Platinum, Thallium, Titanium, Vanadium, and Zinc: Molecular Aspects in Experimental Liver Injury

REMOVAL OF BERYLLIUM (Be2+) FROM WATER SAMPLES BY SORPTION PROCESS: A REVIEW

Hydrogen sulfide alleviates apoptosis and autophagy induced by beryllium sulfate in 16HBE cells

Contact Info

Product

Resources

About