Age-related physiological studies comparing Candida albicans chlamydospores to yeasts

From electron-microscopical observations, a decreased metabolic activity in 3-day-old Candida albicans chlamydospores was suggested, and progressive deterioration in chlamydospores aged 2–8 months was shown. Oxygen utilization by chlamydospore–pseudomycelium (CSP) preparations was less than that by yeast, while 3-day-old CSP preparations used significantly less O2 than 24-h CSP preparations. Amino acid incorporation was greater in yeast than in CSP preparations. Leucine incorporation by 20-h yeasts was twice that of 5-day yeasts and 5 times that of 20-h and 5-day CSP. Amino acid decarboxylation was similar in yeasts and CSP and was determined by end-product analyses to be via amino acid oxidase. Light microscopy autoradiography of [14C]leucine incorporation demonstrated that the metabolic activity in CSP preparations was due to the young growing tips of the pseudomycelium and not to mature chlamydospores. Yeasts did not take up trypan blue but could be stained if first autoclaved or treated with 10% acid or 10% base. Young chlamydospores grown in the presence of trypan blue developed unstained and became permeable to the dye at [Formula: see text] days. These data suggest that chlamydospores of C. albicans do not function in the classical role attributed to spores; i.e., mature chlamydospores cannot germinate, but rather age, deteriorate, and die.

Download Full-text

PEG-fDAO Reduces Lung Inflammation in Chronic Granulomatous Disease Mice Post Challenge with Nonviable Candida Albicans

10.21203/rs.3.rs-216646/v1 ◽

2021 ◽

Author(s):

Hiroyuki Nunoi ◽

Peiyu Xie ◽

Hideaki Nakamura ◽

Yasuaki Aratani ◽

Jun Fang ◽

...

Keyword(s):

Candida Albicans ◽

Amino Acid ◽

Chronic Granulomatous Disease ◽

Lung Inflammation ◽

Acid Oxidase ◽

Granulomatous Disease ◽

Amino Acid Oxidase ◽

Lung Weight ◽

Inflammation Model

Abstract We previously reported that polyethylene glycol-conjugated recombinant porcine D-amino acid oxidase (PEG-pDAO) could supply reactive oxygen species (ROS) to defective NADPH oxidase in neutrophils of patients with chronic granulomatous disease (CGD), and neutrophils regain bactericidal activity in vitro. In the present study, we employed an in vivo nonviable Candida albicans (nCA)-induced lung inflammation model using gp91-phox knockout CGD mice and novel PEG conjugates of Fusarium spp. D-amino acid oxidase (PEG-fDAO), rather than PEG-pDAO. Using three experimentation strategies with the in vivo lung inflammation model, the mouse body weight, lung weight, and lung pathology were evaluated to confirm the efficacy of ROS-generating enzyme replacement therapy with PEG-fDAO. The lung weight and pathological findings were significantly ameliorated by the administration of PEG-fDAO followed by intraperitoneal injection of D-phenylalanine or D-proline. These data suggest that PEG- fDAO with the function of targeted delivery to the nCA-induced inflammation site is applicable in the treatment of inflammation in CGD in vivo.

Download Full-text

PEG-fDAO Reduces Lung Inflammation in Chronic Granulomatous Disease Mice Post Challenge With Nonviable Candida Albicans

10.21203/rs.3.rs-805346/v1 ◽

2021 ◽

Author(s):

Hiroyuki Nunoi ◽

Peiyu Xie ◽

Hideaki Nakamura ◽

Yasuaki Aratani ◽

Jun Fang ◽

...

Keyword(s):

Candida Albicans ◽

Amino Acid ◽

Chronic Granulomatous Disease ◽

Lung Inflammation ◽

Acid Oxidase ◽

Granulomatous Disease ◽

Amino Acid Oxidase ◽

Lung Weight ◽

Inflammation Model

Download Full-text

Purification and Characterization of Lupus Anticoagulant Like Protein from Agkistrodon Halys Brevicaudus Venom

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650698 ◽

1996 ◽

Vol 76 (06) ◽

pp. 0993-0997

Author(s):

Zhao-Yan Li ◽

Xiao-Wei Wu ◽

Tie-Fu Yu ◽

Eric C-Y Lian

Keyword(s):

Amino Acid ◽

Lupus Anticoagulant ◽

Inhibitory Effect ◽

Clotting Factor ◽

Acid Oxidase ◽

Crude Venom ◽

Amino Acid Oxidase ◽

Sds Page ◽

The Individual ◽

Reducing Condition

SummaryBy means of CM-Sephadex C-25, DEAE-Sephadex A-50, Sephadex G-200, and Sephadex G-75 chromatographies, a lupus anticoagulant like protein (LALP) from Agkistrodon halys brevicaudus was purified. On SDS-PAGE, the purified LALP had a molecular weight of 25,500 daltons under non-reducing condition and 15,000 daltons under reducing condition. The isoelectric point was pH 5.6. Its N terminal amino acid sequencing revealed a mixture of 2 sequences: DCP(P/S)(D/G)WSSYEGH(C/R)Q(Q/K). It was devoid of phospho-lipaseA, fibrino(geno)lytic, 5′-nucleotidase, L-amino acid oxidase, phosphomonoesterase, phosphodiesterase and thrombin-like activities, which were found in crude venom. In the presence of LALP, PT, aPTT, and dRVVT of human plasma were markedly prolonged and its effects were concentration-dependent but time-independent. The inhibitory effect of LALP on the plasma clotting time was enhanced by decreasing phospholipid concentration in TTI test. The individual clotting factor activity was not affected by LALP when higher dilutions of LALP-plasma mixture were used for assay. Russell’s viper venom time was shortened when high phospholipid confirmatory reagent was used. Therefore, the protein has lupus anticoagulant property.

Download Full-text

Impairment of Platelet Aggregation by Echis colorata Venom Mediated by L-Amino Acid Oxidase or H2O2

Thrombosis and Haemostasis ◽

10.1055/s-0038-1657280 ◽

1982 ◽

Vol 48 (03) ◽

pp. 277-282 ◽

Cited By ~ 22

Author(s):

I Nathan ◽

A Dvilansky ◽

T Yirmiyahu ◽

M Aharon ◽

A Livne

Keyword(s):

Hydrogen Peroxide ◽

Amino Acid ◽

Platelet Aggregation ◽

Snake Venom ◽

Oxidase Activity ◽

Enzyme Preparation ◽

Acid Oxidase ◽

Crude Venom ◽

Amino Acid Oxidase ◽

Hemostatic Disorders

SummaryEchis colorata bites cause impairment of platelet aggregation and hemostatic disorders. The mechanism by which the snake venom inhibits platelet aggregation was studied. Upon fractionation, aggregation impairment activity and L-amino acid oxidase activity were similarly separated from the crude venom, unlike other venom enzymes. Preparations of L-amino acid oxidase from E.colorata and from Crotalus adamanteus replaced effectively the crude E.colorata venom in impairment of platelet aggregation. Furthermore, different treatments known to inhibit L-amino acid oxidase reduced in parallel the oxidase activity and the impairment potency of both the venom and the enzyme preparation. H2O2 mimicked characteristically the impairment effects of L-amino acid oxidase and the venom. Catalase completely abolished the impairment effects of the enzyme and the venom. It is concluded that hydrogen peroxide formed by the venom L-amino acid oxidase plays a role in affecting platelet aggregation and thus could contribute to the extended bleeding typical to persons bitten by E.colorata.

Download Full-text

Faculty Opinions recommendation of Genetic and physiological data implicating the new human gene G72 and the gene for D-amino acid oxidase in schizophrenia.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1010617.193306 ◽

2003 ◽

Author(s):

Michael O'Donovan

Keyword(s):

Amino Acid ◽

Human Gene ◽

Physiological Data ◽

Acid Oxidase ◽

Amino Acid Oxidase

Download Full-text

Spinal mechanisms contributing to the development of pain hypersensitivity induced by sphingolipids in the rat

Pharmacological Reports ◽

10.1007/s43440-020-00207-x ◽

2021 ◽

Author(s):

Hong Wei ◽

Zuyue Chen ◽

Ari Koivisto ◽

Antti Pertovaara

Keyword(s):

Amino Acid ◽

Nmda Receptors ◽

Receptor Antagonist ◽

Gap Junction ◽

Male Rats ◽

Acid Oxidase ◽

Amino Acid Oxidase ◽

Mk 801 ◽

Mechanical Hypersensitivity ◽

Pain Hypersensitivity

Abstract Background Earlier studies show that endogenous sphingolipids can induce pain hypersensitivity, activation of spinal astrocytes, release of proinflammatory cytokines and activation of TRPM3 channel. Here we studied whether the development of pain hypersensitivity induced by sphingolipids in the spinal cord can be prevented by pharmacological inhibition of potential downstream mechanisms that we hypothesized to include TRPM3, σ1 and NMDA receptors, gap junctions and D-amino acid oxidase. Methods Experiments were performed in adult male rats with a chronic intrathecal catheter for spinal drug administrations. Mechanical nociception was assessed with monofilaments and heat nociception with radiant heat. N,N-dimethylsphingosine (DMS) was administered to induce pain hypersensitivity. Ononetin, isosakuranetin, naringenin (TRPM3 antagonists), BD-1047 (σ1 receptor antagonist), carbenoxolone (a gap junction decoupler), MK-801 (NMDA receptor antagonist) and AS-057278 (inhibitor of D-amino acid oxidase, DAAO) were used to prevent the DMS-induced hypersensitivity, and pregnenolone sulphate (TRPM3 agonist) to recapitulate hypersensitivity. Results DMS alone produced within 15 min a dose-related mechanical hypersensitivity that lasted at least 24 h, without effect on heat nociception. Preemptive treatments with ononetin, isosakuranetin, naringenin, BD-1047, carbenoxolone, MK-801 or AS-057278 attenuated the development of the DMS-induced hypersensitivity, but had no effects when administered alone. Pregnenolone sulphate (TRPM3 agonist) alone induced a dose-related mechanical hypersensitivity that was prevented by ononetin, isosakuranetin and naringenin. Conclusions Among spinal pronociceptive mechanisms activated by DMS are TRPM3, gap junction coupling, the σ1 and NMDA receptors, and DAAO.

Download Full-text