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H Shibata

Publications and source records attributed to H Shibata.

At least 181 records · Page 10Linked to original sources
PubMed1998

Functional analysis of human MLH1 mutations in Saccharomyces cerevisiae.

Hereditary non-polyposis colorectal cancer (HNPCC; OMIM 120435-6) is a cancer-susceptibility syndrome linked to inherited defects in human mismatch repair (MMR) genes. Germline missense human MLH1 (hMLH1) mutations are frequently detected in HNPCC (ref. 3), making functional characterization of mutations in hMLH1 critical to the development of genetic testing for HNPCC. Here, we describe a new method for detecting mutations in hMLH1 using a dominant mutator effect of hMLH1 cDNA expressed in Saccharomyces cerevisiae. The majority of hMLH1 missense mutations identified in HNPCC patients abolish the dominant mutator effect. Furthermore, PCR amplification of hMLH1 cDNA from mRNA from a HNPCC patient, followed by in vivo recombination into a gap expression vector, allowed detection of a heterozygous loss-of-function missense mutation in hMLH1 using this method. This functional assay offers a simple method for detecting and evaluating pathogenic mutations in hMLH1.

Adaptor Proteins, Signal Transducing↗
PubMed1998

Analysis of the structure and substrate binding of Phormidium lapideum alanine dehydrogenase.

The structure of the hexameric L-alanine dehydrogenase from Phormidium lapideum reveals that the subunit is constructed from two domains, each having the common dinucleotide binding fold. Despite there being no sequence similarity, the fold of alanine dehydrogenase is closely related to that of the family of D-2-hydroxyacid dehydrogenases, with a similar location of the active site, suggesting that these enzymes are related by divergent evolution. L-alanine dehydrogenase and the 2-hydroxyacid dehydrogenases also use equivalent functional groups to promote substrate recognition and catalysis. However, they are arranged differently on the enzyme surface, which has the effect of directing opposite faces of the keto acid to the dinucleotide in each case, forcing a change in absolute configuration of the product.

Alanine↗
PubMed1998

Regulatable production of insulin from primary-cultured hepatocytes: insulin production is up-regulated by glucagon and cAMP and down-regulated by insulin.

To utilize hepatocytes for insulin-producing surrogate cells, we devised a regulatory secretion system by placing proinsulin DNA under the regulatable promoter for phosphoenolpyruvate carboxykinase (PEPCK). The expression of PEPCK is down-regulated by insulin, and up-regulated by cAMP and glucagon. To express insulin in hepatocytes, we constructed an adenoviral insulin expression system. After infection, the hepatocytes secreted immunoreactive insulin (IRI) at an increasing rate. IRI secretion increased over four-fold upon stimulation with 300 microM cAMP and 500 microM of the cAMP-dependent phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). This increase was also observed with glucagon and IBMX. Production was augmented two-fold by the addition of wortmannin, phosphatidylinositol (PI)-3-kinase inhibitor, suggesting that inhibitory insulin signaling to the PEPCK promoter may be mediated through PI-3-kinase. Addition of exogenous insulin to the culture decreased insulin mRNA expression remarkably on Northern blot. Thus, by using a PEPCK promoter for insulin expression, we were able to up-regulate insulin production from hepatocytes with cAMP and glucagon, and down-regulate with insulin itself.

1-Methyl-3-isobutylxanthine↗
PubMed1998

Organization of projections of rat retrosplenial cortex to the anterior thalamic nuclei.

The organization of the projections from the retrosplenial cortex (Brodmann's area 29) to the anterior thalamic nuclei was examined in the rat with retrograde transport of the cholera toxin B subunit and anterograde transport of biotinylated dextran amine. Areas 29a and 29b project mainly ipsilaterally to the rostral two-thirds of the anteroventral nucleus, with area 29a projecting more rostrodorsally than area 29b. Area 29c projects bilaterally to the ventromedial part of the anteroventral nucleus. The projections from area 29c are organized in a topographic pattern such that the rostral area 29c projects to the caudoventral part of the anteroventral nucleus, whereas the caudal area 29c projects to the more rostrodorsal parts. Caudal area 29d projects mainly ipsilaterally to the rostrodorsal part of the anteromedial nucleus, and the rostral and dorsal parts of the anteroventral nucleus, whereas rostral area 29d projects bilaterally to the caudodorsal part of the anteromedial nucleus and the caudolateral part of the anteroventral nucleus. All the areas of the retrosplenial cortex provide sparse projections, mainly ipsilateral, to the anterodorsal nucleus, with a crude topographic pattern such that the rostrocaudal axis of the retrosplenial cortex corresponds to the caudorostral axis of the anterodorsal nucleus. The results indicate that each area of the retrosplenial cortex has a distinct projection field within the anterior thalamic nuclei. This suggests that each of these projections transmits distinct information that is important for complex memory and learning functions, e.g. discriminative avoidance learning and spatial memory.

Animals↗
PubMed1998

Biotin status and its correlation with other biochemical parameters in the elderly people of Japan.

OBJECTIVE: Biotin plays important roles in carbohydrate and lipid metabolism as well as in the decarboxylation of amino acids. In this study, to determine the biotin status in elderly people, we determined the levels of biotin and other biochemical variables in their serum. METHODS: Blood was collected from 685 elderly people aged 65 years and over (284 men and 401 women) and from 2,004 reference people. Biotin levels in the serum were microbiologically quantified by the agar plate method and other biochemical variables were recorded using the autoanalyzer. RESULTS: The serum biotin level in elderly people was 10.2 +/- 7.20 pmol/ml (2.5 +/- 1.76 ng/ml), the distribution of which was skewed to the right compared to the reference group (9.4 +/- 1.43 pmol/ml) (2.3 +/- 0.35 ng/ml). However, serum biotin levels did not change with age in the elderly people and no sex-related differences were detected. On the basis of the correlation coefficients among the biochemical variables in the serum, biotin levels were correlated positively with the total cholesterol level. A negative correlation was found between the biotin level and the serum albumin, triiodothyronine, phosphate, and calcium levels. On the other hand, 5.8% of the elderly people had biotinyl IgG in their serum, which did not differ from the percentage in the reference group (4.1%). However, in the elderly people the level of biotinyl IgG positivity was significantly lower in women than in men (4.1% vs. 8.1%). In the biotinyl IgG positive elderly, the levels of parathyroid hormone and total cholesterol were lower, whereas the uric acid level was higher compared to the biotinyl IgG negative elderly. CONCLUSIONS: Although serum biotin levels are not affected by aging, the serum biotin levels of elderly people vary greatly.

Aged↗
PubMed1998

Calcium ion-dependent reactivation of a Pseudomonas lipase by its specific modulating protein, LipB.

LipB, the lipase activator protein of Pseudomonas aeruginosa TE3285, was overproduced in Escherichia coli, and purified 4.9-fold over the crude extract in the presence of SDS. The purified LipB reactivated the lipase from P. aeruginosa TE3285 denatured with guanidine hydrochloride, and its reactivation did not involve multiple turnover. In this reactivation, a 1:1 complex between the lipase and LipB was detected in a cross-linking experiment, suggesting that LipB still binds to the lipase after the reactivation. Calcium ion was essential for the complex formation and the reactivation, and addition of EDTA caused inactivation of the reactivated lipase bound to LipB more rapidly than the native lipase. These findings suggest that LipB could affect the calcium binding to the lipase in the reactivation process. LipB was unable to reactivate lipases from other sources except Pseudomonas sp. 109; this lipase has an amino acid sequence which is 98% identical to that of the lipase from P. aeruginosa TE3285. Thus, it may be concluded that LipB specifically recognizes a unique structural element of the lipase.

Bacterial Proteins↗
PubMed1998

Defective intracellular transport of tissue-nonspecific alkaline phosphatase with an Ala162-->Thr mutation associated with lethal hypophosphatasia.

We have studied the biosynthesis and intracellular transport of tissue-nonspecific alkaline phosphatase (TNSALP) transiently expressed in COS-1 cells. Mutations were introduced into TNSALP to examine the effects of a single amino acid substitution on the activity and biosynthesis of TNSALP. The cells expressing wild-type TNSALP exhibited more than 200-fold higher alkaline phosphatase activity than untransfected ones. Pulse-chase experiments showed that TNSALP was synthesized as a 66-kDa endoglucosaminidase H (Endo H)-sensitive form and converted to EndoH-resistant forms with heterogenous molecular masses ( approximately 80 kDa), which finally appeared on the cell surface as judged by digestion with phosphatidylinositol-specific phospholipase C (PI-PLC). In contrast, a TNSALP with a Glu218-->Gly mutation exhibited no phosphatase activity at all and the 66-kDa Endo H-sensitive form was the only molecular species throughout the chase in the transfected cells. In accordance with this finding, digestion with PI-PLC and immunofluorescence observation confirmed that this mutant was never expressed on the cell surface. Another mutant with a Ala162-->Thr substitution, which naturally occurs in association with a lethal hypophosphatasia, exhibited a low activity and only a small fraction of the 66-kDa form acquired Endo-H resistance and reached the cell surface. Since the wild-type and the mutant TNSALPs were labeled with [3H]ethanolamine, a component of glycosylphosphatidylinositol (GPI), it is unlikely that the impaired intracellular transport of the two mutants is due to a failure in their modification by GPI. Interestingly, the 66-kDa Endo H-sensitive form of the TNSALP mutants but not that of the wild-type, was found to form an interchain disulfide-bonded high-molecular-mass aggregate within the cells. These results suggest that impaired intracellular transport of the TNSALP (Ala162-->Thr) molecule caused by its aggregation is the molecular basis for the lethal hypophosphatasia carrying this mutation.

Alanine↗
PubMed1998

Random mutagenesis on the Pseudomonas lipase activator protein, LipB: exploring amino acid residues required for its function.

LipB, lipase activator protein from Pseudomonas aeruginosa TE3285, specifically recovers the enzymatic activity of denatured inactive lipase. To find important amino acid residues of LipB in this reactivation, random mutagenesis using error-prone PCR was performed on a gene encoding the functional region of LipB. The resultant DNA library was introduced into the lipase expression system using Escherichia coli, and LipB mutants lacking lipase activity were selected by two screening procedures. First, on agar plates containing tributyrin as a substrate for lipase, single colonies lacking active lipase secretion were selected as clones missing the active LipB. Second, to exclude nonsense and frameshift mutants, the molecular size of LipB in the given clones was confirmed by Western blotting. From the selected mutants, of which multiple residues are replaced, five single-residue substituted mutants were newly prepared. Consequently, Y99C, Y99H, S102R and R115C mutants formed no detectable complex with the lipase and lost the in vitro reactivation activity. In the case of Y99C and R115C, their single cysteine residue formed the intermolecular disulfide bridge. Thus, Tyr99 and Arg115 are likely to exist on the molecular surface of LipB, and are candidates for residues that make direct interaction with the denatured lipase in the reactivation process.

Bacterial Proteins↗
PubMed1998

A combination therapy with simvastatin and ursodeoxycholic acid is more effective for cholesterol gallstone dissolution than is ursodeoxycholic acid monotherapy.

Inhibitors of 3-hydroxy,3-methylglutaryl coenzyme A (HMG-CoA) reductase have been reported to decrease the cholesterol saturation index (CSI) in duodenal bile in humans and to prevent formation of cholesterol gallstones in animal studies. We performed a prospective study to evaluate the role of HMG-CoA reductase inhibitors as gallstone-dissolving agents. Fifty patients with radiolucent gallstones in a gallbladder opacifying at drip infusion cholecystography were treated with either 10 mg/day simvastatin plus 600 mg/day ursodeoxycholic acid (group 1, n=26) or 600 mg/day ursodeoxycholic acid alone (group 2, n=24) for 12 months. The ratio of solitary to multiple gallstone cases was 21:29. Plasma lipid levels were assessed and ultrasonographic examination of the gallbladder was performed at baseline and at 3-month intervals during treatment. Duodenal bile sampling was performed in five patients in each group at baseline and after 12 months of treatment. Plasma cholesterol decreased significantly in group 1 but not in group 2. In solitary gallstone cases, no significant difference in dissolution rates was observed between groups 1 (3 of 9, 33%) and 2 (4 of 12, 33%). In contrast, the dissolution rate in multiple gallstone cases was significantly higher in group 1 (12 of 17, 71%) than in group 2 (3 of 12, 25%) (p < 0.01). Bile cholesterol saturation index was significantly decreased (p < 0.01) but did not significantly differ between the two groups. These results suggest that combination therapy with simvastatin and ursodeoxycholic acid is more effective for cholesterol gallstone dissolution than ursodeoxycholic acid monotherapy in patients with multiple gallstones.

Bile↗
PubMed1998

The ecdysteroid UDP-glucosyltransferase gene of Autographa californica nucleopolyhedrovirus alters the moulting and metamorphosis of a non-target insect, the silkworm, Bombyx mori (Lepidoptera, Bombycidae).

The Autographa californica nucleopolyhedrovirus (AcMNPV) does not infect the silkworm and molecular studies on silkworm insusceptibility have not been performed. In cultured cells of the silkworm, the expression of viral genes has been reported. The expression of AcMNPV genes and their effect in vivo and in vitro was studied. In this study, the early gene, the ecdysteroid UDP-glucosyltransferase (egt) gene of AcMNPV, which inactivates the insect moulting hormone by sugar conjugation, was examined to determine whether it would alter the growth of the silkworm. Using wild-type (wt) AcMNPV, the egt gene deletion virus (vEGTDEL), and the virus carrying the egt promoter-lacZ cassette in vEGTDEL (vEGTZ), the egt promoter-driven expression in cultured cells and in nonproductive infection of the silkworm was characterized. Infection of cultured cells with vEGTZ at three different doses occurred in a single cell manner. When budded wt AcMNPV was injected into the fourth and fifth instar larvae, an increase in the amount of virus occurred and caused abnormal larval growth, which resulted in the prolongation or skipping of the larval instar, premature pupation, or death during the pupal stage. For infection of the fourth instar larvae, precocious metamorphosis was observed. When the same amount of vEGTDEL was injected, the alteration of growth did not occur. These results suggest that the egt gene was expressed in the primary infected cells of the silkworm, and that the EGT was secreted into the haemocoel, which significantly altered larval growth.

Animals↗
PubMed1998

Association of a redefined proximal mouse chromosome 11 imprinting region and U2afbp-rs/U2af1-rs1 expression.

Mice with maternal and paternal disomy for chromosome 11 (Chr 11) show growth retarded and overgrowth phenotypes, respectively, which can be attributed to genomic imprinting. Previous studies have defined the region of Chr 11 responsible (the Chr 11 imprinting region) as lying proximal to the T30H translocation breakpoint at the borders of G-bands 11B1.2 and 11B1.3. Evidence is presented here with two new translocations, T57H and T41Ad, which sequentially reduce the size of the imprinting region and locate it proximal to the T41Ad breakpoint in G-band 11A3.2. It therefore lies close to the centromere. The imprinted gene, U2af1-rs1, is known to be located within the original region and has been regarded as a candidate for the imprinting effects. Meiotic and mitotic chromosome FISH analysis, together with U2af1-rs1 expression studies are now described which show that the gene lies within the newly defined imprinting region and that its expression levels relate to the presence/absence and number of functional paternal alleles. U2af1-rs1 therefore remains a candidate gene for the Chr 11 imprinting effects. However, another recently reported imprinted gene, Meg1/Grb10, that lies within the region is also a good candidate, as it encodes a growth factor receptor. Meg1/Grb10 maps about 15 cM from U2af1-rs1 and is separated by conserved regions showing homology with two different human chromosomes. For these reasons, and because the two human homologues of U2af1-rs1 and Meg1/Grb10 also lie on different chromosomes, it would seem likely that the two genes identify two distinct imprinting domains within the small proximal region of mouse Chr 11.

Animals↗
PubMed1998

Activation of calcium-permeable cation channel by insulin in Chinese hamster ovary cells expressing human insulin receptors.

The present study was conducted to examine the ability of insulin receptor to activate the calcium signaling system in Chinese hamster ovary (CHO) cells expressing human insulin receptor (CHO-IR cells). In these cells, insulin evoked the elevation of cytoplasmic free calcium concentration, [Ca2+]c, measured by using fura-2. Insulin-induced increase in [Ca2+]c was blocked by reducing the extracellular calcium concentration to 1 microM or by adding nickel chloride, an inorganic inhibitor of calcium entry. Insulin did not elevate [Ca2+]c in parental CHO cells or in CHO cells expressing mutant insulin receptor lacking an ATP-binding site. When the transmembrane calcium current was measured by perforated whole-cell patch clamp, adding insulin to the bath solution markedly augmented the inward calcium current. In a cell-attached patch, a single channel activity appeared when insulin was included in the pipette. In contrast, insulin added outside the patch was ineffective. The current/voltage relationship demonstrated that insulin activated a voltage-independent calcium-permeable cation channel with a single-channel conductance of 10 pS. Exposing CHO-IR cells to pertussis toxin abolished the subsequent insulin effect on [Ca2+]c and activation of the calcium-permeable channel. Mastoparan activated the 10-pS calcium-permeable cation channel. In an inside-out patch, insulin activated the calcium-permeable channel when the bath solution contained both GTP and ATP. Nonhydrolyzable ATP could substitute for ATP. These results indicate that in CHO-IR cells, insulin elevates [Ca2+]c by activating the 10-pS calcium-permeable cation channel. Activation by the insulin receptor involves pertussis toxin-sensitive G protein.

Adenosine Triphosphate↗
PubMed1998

COUP-TFI expression in human adrenocortical adenomas: possible role in steroidogenesis.

Chicken ovalbumin upstream promoter-transcription factor I (COUP-TFI) is an orphan nuclear receptor essential for neurogenesis, organogenesis, and cell fate determination. CYP17 gene transcription has recently been shown to be activated by SF-1 (steroidogenic factor-1) binding to a cyclic AMP-responsive sequence within the promoter region of the gene, and inhibited by COUP-TF binding to the sequence. Thus, COUP-TF and SF-1 act as a transcriptional repressor and activator, respectively, of CYP17 gene expression. Transcriptional repression by COUP-TFI is mediated by corepressors, N-CoR (nuclear receptor-corepressor) and SMRT (silencing mediator for retinoid and thyroid hormone-receptor), whereas transcriptional activation by SF-1 is mediated by coactivator SRC-1 (steroid receptor coactivator-1). We therefore examined the expression of COUP-TFI, SF-1, SRC-1, N-CoR, and SMRT in a variety of adrenocortical adenomas and compared the results with CYP17 mRNA levels. We found significantly high COUP-TFI mRNA expression in nonfunctional adenomas (n=8: 220+/-16%; normal 96+/-4%), a deoxycorticosterone-producing adenoma (n=1: 200%), and a pre-clinical Cushing's adenoma (n=1: 280%), intermediate COUP-TFI expression in cortisol-producing adenomas (n=8: 63+/-5%), and low COUP-TFI expression in aldosterone-producing adenomas (n=8: 49+/-4%). In contrast to COUP-TFI, SF-1 mRNA expression did not vary significantly among adrenals. We did not detect the expected negative correlation between COUP-TFI and CYP17 mRNA levels in adrenocortical adenomas. High COUP-TFI expression was associatedwith a nonfunctioning phenotype. Interestingly, the pattern of COUP-TFI expression was similar to the profile of N-CoR expression, but not of SMRT expression. These results indicate that COUP-TFI and N-CoR may play a role in steroidogenesis by human adrenocortical adenomas.

Adenoma↗
PubMed1998

Expression of low-molecular-weight kininogen in mouse vascular smooth muscle cells.

To determine the existence of the kallikrein-kinin system in vascular wall, the expression of low-molecular-weight (LMW) kininogen, a precursor protein of kinins, was studied in mouse aortic smooth muscle in vivo or in cultured vascular smooth muscle cells (VSMC) derived from mouse aorta in vitro. Although LMW-kininogen mRNA was undetectable in aortic smooth muscle of untreated mice using either Northern blotting or reverse transcription-polymerase chain reactions (RT-PCR) followed by Southern blotting, administration of lipopolysaccharide (LPS; 1 mg/kg, i.v.) induced the expression of LMW-kininogen mRNA at levels detectable by RT-PCR within 12 h. Cultured VSMC not only expressed LMW-kininogen mRNA at levels easily detectable by RT-PCR, but also secreted LMW-kininogen-like protein that was immunoreactive to anti-mouse LMW-kininogen antibody. These results demonstrate that VSMC are a source of LMW-kininogen in the mouse, and suggest the presence of a local kallikrein-kinin system in vascular tissue. LPS-induced up-regulation of LMW-kininogen expression suggests a role for vascular LMW-kininogen in tissue trauma or inflammation.

Animals↗
PubMed1998

Synthesis and biological evaluation of phenylacetyl derivatives having low central nervous system permeability as potent and selective M2 muscarinic receptor antagonists.

A series of phenylacetyl derivatives containing the 5,10-dihydro-11H-dibenzo[b,e,][1,4]diazepin-11-one or 5,11-dihydro-6H-pyrido[2,3-b][1,4]benzodiazepin-6-one skeleton was prepared and evaluated for their binding affinities to muscarinic receptors in vitro and for antagonism of bradycardia, salivation and tremor in vivo. Among them, compounds 56 and 66 had high affinity for M2 muscarinic receptors in the heart (pKi = 8.7 and 8.9, respectively) with low affinity for M3 muscarinic receptors in the submandibular gland. A structure-activity relationship (SAR) study suggested that the high M2 selectivity over the M3 muscarinic receptors of 56 may be attributed to the direction of the carboxamide carbonyl group. In in vivo studies, 56 and 66 antagonized oxotremorine-induced bradycardia in rats on both intravenous and oral administration, and their heart rate increasing effect in dogs with nocturnal bradycardia was about 3-fold greater than that of AF-DX 116. Furthermore, they had almost no influence on oxotremorine-induced tremor in mice, presenting no evidence of central transfer.

Animals↗
PubMed1998

[Synthesis and antiulcer activity of N-2-(2-hydroxy-2-phenyl)ethyl-N"-(methanesulfonyl)guanidine analogue of ranitidine. Development of a new antiulcer agent T-593].

A series of the aryl-substituted N'-2-(2-hydroxy-2-phenyl)ethyl derivatives of N"-methanesulfonyl-N-2-((5-dimethylaminomethyl or 5-methylaminomethyl) furfurylthio)ethylguanidine have been synthesized as potential antisecretory and mucosal protective antiulcer agents. The synthetic routes involves, at the last stage, the reaction of 2-hydroxy-2-phenylethylamines with N-2-(furfurylthio)-ethyl-N'-methanesulfonyl-S-methylisothiourea or its O-phenylisourea counterpart. The primary screening test to assess the inhibitory activity of the synthetic compounds on histamine-induced gastric acid secretion was carried out in anesthetized rats by the lumen-perfusion technique of Ghosh and Schild and also by the pylorus-ligated preparation method. The best profile of histamine H2-antagonist activity was much better than that of the prototype ranitidine, and obtained with N'-(2-(2-hydroxy-2-(4-hydroxyphenyl)) ethyl-N"-methanesulfonyl-N-2-(5-(methylaminomethyl)furfurylthio)et hylguanidine (12f), which was also characterized by enhancing the gastric mucosal blood flow in rabbits as observed by the thermoelectric method. This compound 12f, designated as T-593, significantly inhibited the formation of the indomethacin-induced gastric lesions in rats; 3.5-fold more potent than ranitidine, but 4-fold less active than famotidine. On the other hand, T-593 and famotidine displayed comparable activities in healing the acetic acid-induced gastric ulcer with and without the dosing of indomethacin. Additional notable features of T-593, as determined in rats, are that its protective effect on the hemorrhagic shock-induced lesion under the prior dosing of histamine is ca. 10- and 2-fold greater than ranitidine and famotidine, respectively, and that a decrease in the gastric mucosal blood flow caused by a partial blood-withdrawal is more strongly recovered with T-593 than with famotidine. These experimental results suggest that the antiulcer efficacy of T-593 can be explained by its dual activities: antisecretion of gastric acid and, more importantly, protection of gastric mucous membrane.

Animals↗
PubMed1998

Iron chelation by chlorogenic acid as a natural antioxidant.

Chlorogenic acid, a dietary antioxidant, effectively inhibited the iron-induced lipid peroxidation of bovine liver microsomes in a concentration-dependent manner. In the Fenton-type reaction, chlorogenic acid inhibited the production of the hydroxyl radical by iron-EDTA or iron-ADP, while iron plus chlorogenic acid did not generate the hydroxyl radical. The formation of an iron complex with chlorogenic acid was demonstrated by UV/vis absorbance spectroscopic, ESR and 1H-NMR studies. The ferric complex with chlorogenic acid was in the ferric high-spin state near rhombicity, and had no radical scavenging activity. The results indicate that chlorogenic acid prevented the formation of the hydroxyl radical by forming a chelate with iron whose complex cannot catalyze the Fenton-type reaction.

Animals↗