1.
Hydrogen sulfide regulates the activity of antioxidant enzymes through persulfidation and improves the resistance of tomato seedling to Copper Oxide nanoparticles (CuO NPs)-induced oxidative stress.
Li, J, Shi, C, Wang, X, Liu, C, Ding, X, Ma, P, Wang, X, Jia, H
Plant physiology and biochemistry : PPB. 2020;:257-266
Abstract
Hydrogen sulfide (H2S), a small gaseous signaling molecule, regulates antioxidase activity and improves plant tolerance to oxidative stress. The phytotoxic effect of Copper Oxide (II) nanoparticles (CuO NPs) is due to oxidative stress. Here, we show that H2S-mediated persulfidation of antioxidase is essential for an effective stress response of tomato exposed to CuO NPs. The CuO NP-induced increase in hydrogen peroxide (H2O2) and malondialdehyde (MDA) levels was significantly reduced by treatment with the H2S donor NaHS. In vivo, NaHS increased superoxide dismutase (SOD), ascorbate peroxidase (APX) and peroxidase (POD) activities under CuO NP stress. In vitro, NaHS increased APX and POD activities but decreased catalase (CAT) activity. Persulfidation existed in recombinant SlCAT1, SlcAPX1 and SlPOD5 proteins. The persulfidatied cysteine (Cys) residues were verified by liquid chromatography-tandem mass spectrometry (LC-MS/MS), revealing their position on the protein surface. Cys234 of SlCAT1 is located in the immune-responsive domain and close to the enzyme activity domain. Cys234 of SlcAPX1 and Cys 61 SlPOD5 are located in the enzyme activity domain. Persulfidation increased SlcAPX1 and SlPOD5 activities but decreased SlCAT1 activity. These data indicate that H2S-mediated persulfidation posttranslationally regulates the activities of CAT, APX and POD, thereby enhancing the plant's response to oxidative stress. Additionally, this work provides an experimental approach for the study of persulfidation in plants.
2.
Handling of nutrient copper in the bacterial envelope.
Stewart, LJ, Thaqi, D, Kobe, B, McEwan, AG, Waldron, KJ, Djoko, KY
Metallomics : integrated biometal science. 2019;(1):50-63
Abstract
In bacteria, copper (Cu) is often recognised for its potential toxicity and its antibacterial activity is now considered a key component of the mammalian innate immune system. Cu ions bound in weak sites can catalyse harmful redox reactions while Cu ions in strong but adventitious sites can disrupt protein or enzyme function. For these reasons, the outward transport of Cu from bacteria has received significant attention. Yet, Cu is also a bacterial nutrient, required as a cofactor by enzymes that catalyse electron transfer processes, for instance in aerobic and anaerobic respiration. To date, the inward flow of this metal ion as a nutrient and its insertion into target cuproenzymes remain poorly defined. Here we revisit the available evidence related to bacterial nutrient Cu trafficking and identify gaps in knowledge. Particularly intriguing is the evidence that bacterial cuproenzymes do not always require auxiliary metallochaperones to insert nutrient Cu into their active sites. This review outlines our effort to consolidate the available experimental data using an established energy-driven model for metalation.
3.
The Role of Copper Homeostasis at the Host-Pathogen Axis: From Bacteria to Fungi.
Li, C, Li, Y, Ding, C
International journal of molecular sciences. 2019;(1)
Abstract
Copper is an essential trace element participating in many vital biological processes, however it becomes a toxic agent when in excess. Thus, precise and tight regulation of copper homeostasis processes, including transport, delivery, storage, detoxification, and efflux machineries, is important, ensuring that only the amount needed to sustain basic biological functions and simultaneously prevent copper toxicity in the cell is maintained. Numerous exciting studies have revealed that copper plays an indispensable role at the microbial pathogen-host axis for entities ranging from pathogenic bacteria to deadly fungal species. Analyses of copper homeostases in bacteria and fungi extensively demonstrate that copper is utilized by the host immune system as an anti-microbial agent. The expression of copper efflux and detoxification from microbial pathogens is induced to counteract the host's copper bombardment, which in turn disrupts these machineries, resulting in the attenuation of microbial survival in host tissue. We hereby review the latest work in copper homeostases in pathogenic bacteria and fungi and focus on the maintenance of a copper balance at the pathogen-host interaction axis.
4.
Copper Deficiency: Causes, Manifestations, and Treatment.
Altarelli, M, Ben-Hamouda, N, Schneider, A, Berger, MM
Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition. 2019;(4):504-513
Abstract
BACKGROUND The metabolism of the essential trace element copper remains incompletely understood and, until recently, nearly ignored in acute medicine. Menkes disease was for long the only known copper deficiency condition, but several case reports and investigations conducted over the last 2 decades have shown that deficiency is more frequent than previously suspected, with devastating individual consequences and potential public health consequences. The copper needs in healthy individuals are 0.9 mg/d, which translates to 0.3 mg/d intravenously in parenteral nutrition; the present review aims at gathering actual knowledge. METHOD AND RESULTS A review of literature was conducted in PubMed and Cochrane systematic reviews to identify the most recent information about copper deficiency and generate a narrative review. Copper deficiency has hereditary and acquired origins, the latter being the most frequent. Clinical manifestations are nonspecific but affect all organs and systems, particularly the hematologic (anemia) and the neurologic (myeloneuropathy) systems. Deficiency also affects the cardiovascular, cutaneous, and immune systems. Severe copper deficiency due to reduced absorption after bariatric bypass surgery has become frequent. CONCLUSION Deficiency is more frequent than previously recognized, probably because of changing nutrition patterns but also because of some treatments that have become very common such as bypass bariatric surgery and, in acute medicine, prolonged continuous renal replacement therapy. The patients may present with severe hematologic and neurologic complications that go untreated because copper deficiency was not considered in the differential diagnosis: These complications often need active intravenous repletion with doses 4-8 times the usual nutrition recommendations.