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Application of emerging technologies in the antiviral field.

Viral diseases pose a serious threat to global public health, agriculture, and biosecurity. Conventional antiviral strategies are often limited by an incomplete understanding of disease mechanisms, poor targeting precision, and slow response times. Emerging technologies are now reshaping the landscape of antiviral research. This review examines the roles of four key frontiers, including organoid models, gene editing, AI-driven molecular design, and synthetic biology. Organoids provide physiologically relevant platforms that model virus-host interactions and disease progression. Viral infections remain a major challenge to human and animal health, agriculture, and biosecurity. Progress in antiviral research is constrained by the complexity of viral pathogenesis, the diversity and rapid evolution of viruses, and the limited translational relevance of some traditional model systems. Recent advances in organoid technology, gene editing, artificial intelligence, and synthetic biology are expanding the toolkit available for antiviral research and development. In this review, we discuss how these four technological frontiers contribute to disease modeling, target discovery, molecular design, and translational innovation. Organoids, in particular, provide physiologically relevant systems for investigating viral infection, tissue tropism, host responses, and pathogenesis. Gene editing tools, such as CRISPR, enable precise manipulation of host and viral genomes, facilitating the development of resistant organisms and next-generation vaccine platforms. AI technologies, including AlphaFold for structure prediction and platforms for de novo protein design, address long-standing bottlenecks in structural biology and offer powerful means to engineer antiviral proteins, antibodies, and vaccine antigens. Synthetic biology, guided by the Design-Build-Test-Learn cycle, integrates computational design, genetic assembly, and functional validation into a cohesive pipeline. Together, these technologies form a synergistic workflow that spans disease modeling, target discovery, molecular design, construction, testing, and iterative optimization. This integrated approach is shifting antiviral development from traditional empirical methods toward more precise, intelligent strategies. The review also highlights ongoing challenges in integration and scalability, stressing that high-quality biological datasets and stronger interdisciplinary collaboration are essential for realizing translational potential. By presenting a cohesive view of these converging methodologies, this review offers a framework to guide the intelligent evolution of antiviral strategies in both human and animal health.

Antiviral

Development of molecular markers associated with saline-alkali tolerance in rapeseed (Brassica napus L.).

A total of 947 saline-alkaline tolerance-related molecular markers and a 5K cGPS genotyping chipwere developed, providing practical tools for marker-assisted selection and molecular design breeding of saline-alkaline-tolerant rapeseed. Rapeseed (Brassica napus L.) has relatively strong tolerance to saline-alkaline stress and shows great potential for the sustainable utilization and improvement of saline-alkaline soils. However, the breeding of highly tolerant cultivars still mainly depends on conventional hybridization combined with phenotype-based selection, which constrains breeding efficiency. In this study, previously reported saline-alkaline tolerance-related genes from rapeseed, rice, maize, wheat, sorghum, and Arabidopsis were collected. Candidate gene-based association analysis enabled the development of molecular markers and a genotyping chip. A total of 483 significantly associated genes were identified, among which 355 genes contained favorable haplotypes. Molecular markers were successfully developed for 275 genes, including 746 KASP and 201 InDel marker pairs, and four marker pairs were randomly selected for validation. In addition, a 5K cGPS liquid-phase chip (HZSW-cGPS-BRNAP-04), was developed and showed a high call rate and excellent reproducibility in genotyping. These markers and the chip are expected to improve the breeding efficiency of saline-alkaline-tolerant rapeseed cultivars. Overall, this study provides useful tools for early-generation evaluation and marker-assisted selection (MAS), and provides a foundation for molecular design breeding of saline-alkali-tolerant rapeseed.

Brassica napus

Design of molecular control mechanisms and the demand for gene expression.

Regulation by a repressor protein is the mechanism selected when, in the organism's natural environment, there is low demand for expression of the regulated structural genes. Regulation by an activator protein is selected when there is high demand for expression of the regulated structural genes. These general conclusions are useful in relating physiological function to underlying molecular determinants in a wide variety of systems that includes repressible biosynthetic pathways, inducible biosynthetic enzymes, inducible drug resistance, and prophage induction, as well as inducible catabolic pathways, for which a special case of this prediction previously was reported [Savageau, M. A. (1974) Proc. Natl. Acad. Sci. USA 71, 2453-2455].

Bacteria

Dual recognition drives site-directed G-quadruplex stabilization: Oligonucleotide design in G4 ligand-oligonucleotide conjugates.

G-quadruplex (G4) DNA structures are increasingly recognized for their roles in transcriptional regulation and genome stability, making them attractive therapeutic targets. Selective recognition of individual G4s remains challenging due to the high structural similarity among G4 motifs. G4 Ligand-Oligonucleotides conjugates (GL-Os) address this challenge by combining small-molecule G4 ligands with the sequence specificity of oligonucleotides, targeting sequences flanking the intended G4 target. Here, we systematically investigate how oligonucleotide length, backbone composition, and sequence complementarity govern GL-O binding, selectivity, and G4 stabilization. We show that effective G4 recognition depends on the interdependence between oligonucleotide hybridization and G4 ligand binding, such that both elements cooperatively reinforce complex stability and site specificity. Longer oligonucleotides promote more stable complexes and stronger G4 stabilization, whereas central mismatches disrupt this dual-recognition mechanism. Replacement of DNA with peptide nucleic acids (PNAs) enhances binding strength, thermal stability, and metabolic stability. Importantly, ligand conjugation redirects PNA oligonucleotides from nonspecific polymerase stalling toward selective G4 stabilization. Finally, we demonstrate receptor-mediated cellular uptake of modified GL-Os, supporting the feasibility of cellular delivery while highlighting remaining delivery barriers. Together, these findings show the molecular design principles governing GL-O behavior and provide a foundation for the future development and evaluation of selective G4-targeting therapeutics.

G-quadruplex DNA

Research progress on the regulatory mechanisms of the PSY promoter.

Carotenoids are essential pigments in the plant photosynthetic apparatus, functioning in light harvesting, photoprotection, and signal transduction, and serving as precursors of vital nutrients such as vitamin A. Phytoene synthase (PSY) is the first rate-limiting enzyme in the plant carotenoid biosynthetic pathway, and its transcriptional regulation primarily depends on cis-acting promoter elements, associated transcription factors, and epigenetic status. The PSY promoter region contains core cis-elements as well as multiple light-, hormone-, and stress-responsive elements, which collectively function as key regulatory sites governing spatiotemporal expression. This review systematically summarizes recent advances in PSY promoter regulation by plant hormones (e.g., abscisic acid, ethylene, jasmonic acid), environmental factors (light signaling, temperature, salinity, and drought), and epigenetic mechanisms (DNA methylation, histone modifications, and chromatin remodeling). In addition, the application of transgenic and biotechnological approaches to PSY promoter regulation is further summarized. Including promoter sequence engineering with precise editing of cis-elements and promoter-targeted CRISPR activation/interference (CRISPRa/i) for tunable transcriptional control. Emphasis is placed on how these signals are integrated at the promoter level. Deeper insights into these mechanisms will provide both theoretical foundations and practical strategies for enhancing carotenoid accumulation and stress tolerance in crops through molecular design.

Promoter Regions, Genetic

LCORL and STC2 Variants Increase Body Size and Growth Rate in Cattle and Other Animals.

Natural variants can significantly improve growth traits in livestock and serve as safe targets for gene editing, thus being applied in animal molecular design breeding. However, such safe and large-effect mutations are severely lacking. Using ancestral recombination graphs, we investigated recent selection signatures in beef cattle breeds, pinpointing sweep-driving variants in the LCORL and STC2 loci with notable effects on body size and growth rate. The ACT-to-A frameshift mutation in LCORL occurs mainly in central-European cattle, and stimulates growth. Remarkably, convergent truncating mutations were also found in commercial breeds of sheep, goats, pigs, horses, dogs, rabbits, and chickens. In the STC2 gene, we identified a missense mutation (A60P) located within the conserved region across vertebrates. We validated the two natural mutations in gene-edited mouse models, where both variants in homozygous carriers significantly increase the average weight by 11%. Our findings provide insights into a seemingly recurring gene target of body size enhancing truncating mutations across domesticated species, and offer valuable targets for gene editing-based breeding in animals.

Animals

Artificial Intelligence for Natural Products Discovery and Development.

Natural products (NPs) remain a cornerstone of modern drug discovery, offering stereochemical complexity and diverse bioactivities that precisely modulate therapeutic targets, refined through billions of years of evolution. However, their research has long been hindered by inefficient, empirical workflows, high resource consumption, structural complexity, and the "multicomponent, multi-target" nature of their mechanisms. The exponential growth of genomic, metabolomic, and spectral data has overwhelmed conventional analytical methods, exposing critical bottlenecks in handling high-dimensional, heterogeneous datasets that exceed human interpretive capacity. Artificial intelligence (AI) is emerging as a transformative paradigm to address these challenges, integrating multi-omics and chemical data to shift NP research from fragmented empiricism toward mechanism-driven, precision-oriented development. By leveraging deep learning architectures- including graph neural networks, Transformers, and diffusion-based generative models-AI enables systematic decoding of NP biosynthesis, automated structure elucidation, rational target identification, knowledge extraction from vast unstructured scientific literature, and de novo molecular design. This review comprehensively surveys recent advances in AI applications across the full NP discovery and development pipeline, encompassing genome mining, structure-based and ligand-based virtual screening, multimodal structural characterization, lead optimization, and biosynthetic pathway engineering. We further examine the emerging roles of protein-centric, molecule- centric, and multimodal foundation models, as well as large language models, in bridging genotype-to-chemotype gaps and unlocking unstructured scientific knowledge. Finally, we discuss critical challenges including data scarcity, representational limitations for complex stereochemistry, physical plausibility in generative models, and the urgent need for experimental validation, while outlining future directions toward autonomous experimentation, closed-loop optimization, and human-AI collaborative discovery.

Artificial intelligence

Molecular Bases and Genetic Design of Rice Disease Resistance for Optimized Yield and Sustainable Agriculture.

Rice diseases continue to undermine yield stability and threaten the sustainability of rice production. The central challenge is therefore not simply to maximize immune activation, but to identify genetic interventions that remain effective across diverse pathogen races and environmental conditions without imposing excessive penalties on growth or yield. Here, we synthesize the molecular basis of rice immunity from a design-oriented perspective. We first examine cell-surface pattern-recognition receptors and intracellular nucleotide-binding leucine-rich repeat receptors, and then assess the shared signaling hubs and defence outputs that connect pathogen perception to antimicrobial responses. Rather than treating these components as equivalent breeding targets, we compare their translational potential according to resistance spectrum, anticipated durability, tunability, pleiotropic risk, and the strength of field evidence. We further discuss breeding strategies based on receptor engineering, editing of susceptibility genes and cis-regulatory elements, post-translational motif engineering, pathogen-inducible and upstream open reading frame-mediated regulation, resistance-gene stacking and artificial intelligence-assisted prediction. We argue that rational resistance design in rice should move beyond constitutive immune activation toward allele-specific, quantitative, spatially restricted and infection-responsive regulation. Integrating mechanistic insights with precision genome editing, accelerated breeding and responsible deployment offers a practical route to durable, yield-compatible disease resistance while reducing dependence on chemical control.

breeding strategy

Purification, separation, and characterization of two molecular forms of D-1-amino-2-propanol:NAD+ oxidoreductase activity from extracts of Escherichia coli K-12.

D-1-Amino-2-propanol:NAD+ oxidoreductase activity, which catalyzes the second step in a pathway wherein L-threonine is converted to D-1-amino-2-propanol via the intermediate formation of aminoacetone, has been purified 500-fold from Escherichia coli K-12. Although the enzyme catalyzes the oxidation of certain diols as well as 1-amino-2-propanol, it is completely specific for the D-isomer of the amino alcohol and for NAD+. Two molecular forms (designated Form L and Form S) of the oxidoreductase, both of which are catalytically active, have been separated by gel filtration on Sephadex G-200; apparently, Form L is converted to Form S by dissociation (Form L leads to Form S). Molecular weight determinations indicate that the two forms of the enzyme are different not only in size but also in shape; Form L apparently is an asymmetric tetramer of Form S. The two molecular species have similar catalytic properties. Both exhibit the same pH optimum of 8.6, have nearly identical apparent Km values for substrate and cosubstrate, are equally sensitive to inhibition by p-mercuribenzoate and N-ethylmaleimide, and show the same specificity for cosubstrate. Neither form of the enzyme has an absolute requirement for added thiol compounds or divalent metal ions.

Alcohol Oxidoreductases

Fractionation and properties of glucans produced by Streptococcus mutans.

Water-insoluble (ISG) and water-soluble (SG) fractions of glucans produced by cell-free glucosyltransferase of Streptococcus mutans AHT (serotype g) were isolated by centrifugation at 20,000 x g for 15 min. No further resolution of slightly sonicated ISG was observed with gel filtrations on any Bio-Gel beads, including A-50m. Bio-Gel P-100 filtration subdivided SG into two fractions with higher and lower molecular weights (designated SG-A and SG-B, respectively). SG-A was further resolved into two subfractions, SG-A-I and SG-A-II, by 10 to 40% and 50 to 80% ethanol precipitation, respectively. Relative amounts of ISG, SG-A-I, SG-A-II, and SG-B were 66.3:9.4:4.4:19.9. The molecular sizes of these fractions were >1.5 x 10(7), >==1.5 x 10(7), <==5 x 10(6) (>1 x 10(5)), and <==1 x 10(4) daltons, and their alpha-1,3 glucosidic linkage contents were approximately 35, 35, 16, and 4% for fractions ISG, SG-A-I, SG-A-II, and SG-B, respectively. Both ISG and SG-A-I were resistant to hydrolysis by dextranase and possessed the ability to aggregate with concanavalin A and to agglutinate S. mutans cells. SG-A-II had extremely low dextranase susceptibility and significant agglutinating activities, whereas SG-B showed high dextranase sensitivity and neither aggregating nor agglutinating activity. These results indicate that SG of S. mutans AHT consists of three types of glucans with distinctly different molecular sizes and chemical structures and strongly suggest that the ISG and SG-A-I fractions are different physical states of an inherently identical glucan. Preliminary observations suggest that the glucans produced by other S. mutans strains of several serotypes may be similarly classified.

Agglutination

Virus-specific protein synthesis in cells infected by infectious pancreatic necrosis virus.

A study of virus-specific protein synthesis in infectious pancreatic necrosis virus-infected RTG-2 cells was undertaken to find a relationship between the coding capacity of virus genome (two segments of double-stranded RNA of 2.5 X10(6) and 2.3 X 10(6) molecular weight) and the sizes and relative amounts of polypeptides in the virion and in infected cells. The time course of virus-specific protein synthesis was followed by pulse labeling infected UV-irradiated cells with [35S]methionine and analyzing the labeled proteins by polyacrylamide gel electrophoresis followed by autoradiography. Three size classes of virus-specific polypeptides were synthesized, in the same relative proportion, throughout the infectious cycle, beginning 3 h postinfection. Their designation and molecular weight was as follows: alpha1, 1000,000; alpha2, 90,000; beta1, 59,000; beta2, 56,000; gamma1, 32,000; gamma2, 30,000; and gamma3, 28,000. Experiments using amino acid analogues, protease inhibitors, ZnCl2, and supraoptimal temperatures showed that polypeptides of the beta and gamma families did not arise from the alpha polypeptides by post-translational cleavage. Slow cleavage late in the infectious cycle could be demonstrated, since during 12-h period radioactivity was chased from beta1 via beta3 to beta4 (molecular weight 50,000) and beta5 (molecular weight, 49,000). During the chase most of gamma2 was degraded, whereas radioactivity could not be chased from the remaining virus-specific polypeptides. Purified virus contained polypeptides alpha1, alpha2, beta4, beta5, and gamma1. The beta polypeptides made up over 60% of the virion proteins. The results suggest that infectious pancreatic necrosis vibrus possesses a unique mechanism for synthesis of three size-classes of proteins using mRNA transcripts from two high-molecular-weight double-stranded RNA genome segments.

Animals

Molecular diagnostic yield and barriers in inherited retinal diseases: a retrospective cohort study.

OBJECTIVE: To evaluate the diagnostic yield of panel-based genetic testing for inherited retinal diseases (IRDs) and identify barriers to molecular resolution. DESIGN: Retrospective cohort. PARTICIPANTS: A total of 404 patients with clinically confirmed IRDs who were evaluated at the Adult Inherited Retinal Dystrophy Service, Ontario, Canada (October 2021-September 2024). METHODS: Patients underwent targeted massive parallel sequencing panel testing. Diagnostic yield was calculated, and unresolved cases were reviewed. Associations between yield, phenotype, ethnicity, and sex were assessed using &#x3c7;&#xb2; analysis. RESULTS: Of 685 referrals, 570 had confirmed IRDs. After we excluded 140 pending results and 26 patients who declined testing, 404 patients were analyzed. At referral, 94 patients (23.2%) had a previous molecular diagnosis, and 138 (34.0%) were diagnosed through clinic-initiated testing, giving an overall yield of 57.4%. Yield varied significantly by phenotype (&#x3c7;&#xb2;, P&#x202f;=&#x202f;1.4&#x202f;&#xd7;&#x202f;10&#x207b;&#x2076;), from 94.4% in vitelliform macular dystrophies to 25.0% in vitreoretinopathies, with no sex association (P&#x202f;=&#x202f;1.0). Disease-causing variants were identified in 83 IRD-associated genes, most frequently ABCA4, USH2A, and BEST1. Of 172 unresolved cases, 62 (36.0%) had negative panels, and 110 (63.9%) were inconclusive, including 30 with unphased pathogenic variants in recessive genes and 10 with high-suspicion variants of uncertain significance. Key barriers included limited family availability for phasing, restricted access to functional assays, and lack of public coverage for whole-exome or whole-genome sequencing. CONCLUSIONS: Massive parallel sequencing-based panel testing achieved a 57% diagnostic yield in this IRD population. Success was strongly phenotype-dependent with substantial heterogeneity. Whole-exome sequencing, whole-genome sequencing, family segregation, and functional genomics could improve diagnostic outcomes and management.

Humans

Multiple molecular forms of catechol-O-methyltransferase. Evidence for two distinct forms, and their purification and physical characterization.

Catechol-O-methyltransferase (COMT: EC 2.1.1.6) has been shown to exist in the soluble fraction of rat liver as two distinct molecular forms, designated COMT I and COMT II, which are separable by gel filtration, ion exchange chromatography, and sedimentation. The predominant form, COMT I, has a smaller Mr of about 24,000, as determined by gel filtration and sedimentation, and less negative charge, whereas the minor form, COMT II, has a larger Mr of about 47,500 and more negative charge. The COMT I and COMT II have been purified 450- and 205-fold, respectively, from rat liver by a newly developed procedure which gives homogeneous enzyme preparations with respect to catechol-methylating activities. The molecular properties of the predominant form, COMT I, were: s20,w, 2.7; D20,W, 10.5; Stokes radius, 20.1 A; f/fo, 1.08; and pI, 4.9. For the minor form, COMT II, the values were s20,w, 3.8; D20,w, 7.3; Stokes radius, 28.7 A; f/fo, 1.23; and pI, 4.8. Catechol-O-methyltransferase was found to exhibit tissue-specific isozymic patterns in the distribution of its two variant forms. In the rat tissues, the liver and kidney exhibited the presence of the two physically separable forms. Catechol-O-methyltransferase was also found as two distinct molecular forms in human tissues, including liver, brain, and placenta. The two forms of human catechol-O-methyltransferase were not distinguishable by the criteria of gel filtration from their counterparts in rat liver, indicating that the two molecular forms of human and rat liver catechol-O-methyltransferase are homologous. No interconversion of one molecular form of catechol-O-methyltransferase into the other was observed under experimental conditions employed. Available evidence indicates that the two molecular forms of catechol-O-methyltransferase are genetically dissimilar proteins.

Animals

Effects of umbilical cord mesenchymal stem cell-derived exosomes on periodontal ligament stem cells: An exploratory study.

OBJECTIVE: To investigate whether exosomes derived from human umbilical cord mesenchymal stem cells (UCMSCs) at two osteogenic induction stages (undifferentiated and late-stage) differentially affect periodontal ligament stem cells (PDLSCs), and to explore the potential molecular basis. DESIGN: UCMSCs and PDLSCs were isolated and cultured. Exosomes were harvested from undifferentiated UCMSCs (Exo-D0) and UCMSCs after 14 days of osteogenic induction (Exo-D14). PDLSCs were treated with both exosome types. Proliferation and migration were analyzed using EdU and scratch assays, the latter under serum-free conditions. Early osteogenic differentiation was assessed by alkaline phosphatase staining and quantitative reverse transcription PCR (qRT-PCR). Differentially expressed miRNAs were identified by high-throughput sequencing and further analyzed through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. RESULTS: Both exosome types promoted PDLSC migration. Exo-D0 enhanced early osteogenic differentiation, whereas Exo-D14 enhanced proliferation but reduced early osteogenic marker expression. Sequencing identified 21 differentially expressed miRNAs (13 upregulated, 8 downregulated). Bioinformatic prediction suggested that the putative target genes were enriched in Ras signal transduction, regulation of kinase activity, and focal adhesion, and further predicted significant enrichment in the MAPK, Ras, and PI3K-Akt signaling pathways, which are central to cell proliferation and osteogenic differentiation. CONCLUSIONS: Exosomes from undifferentiated and osteogenically induced UCMSCs exerted distinct effects on PDLSCs, potentially associated with differentially packaged miRNAs. These findings offer a basis for hypotheses about exosome-mediated mechanisms and support matching exosome sources to the intended therapeutic outcome as potential cell-free strategies for periodontal tissue regeneration and alveolar bone repair.

Humans

Identification of prelarge and presmall basic proteins in mouse myelin and their structural relationship to large and small basic proteins.

A new technique is described to identify antigenically related proteins by radioimmunoassay after sodium dodecyl sulfate/polyacrylamide gel fractionation. When adult mouse myelin was examined by this technique, four proteins that are antigenically related to the small myelin basic protein were identified. They were designated: prelarge (molecular weight 21,500), large (18,500), presmall (17,000), and small (14,000). The four proteins were isolated by elution from polyacrylamide gels, and each protein migrated as a single band when analyzed by either sodium dodecyl sulfate or acidic polyacrylamide gel electrophoresis. Serial dilutions of the purified proteins were measured by radioimmunoassay. Both the slope of the inhibition curve and the level of maximal inhibition for each protein were the same as for the small myelin basic protein, indicating that each of the four proteins contains all of the antigenic sites present in the small basic protein. Structural relationships among the four proteins were examined by using two-dimensional analysis of tryptic digests. The results showed that: large was similar in amino acid sequence to the major myelin basic protein from other species; small was identical in sequence to large, except for an internal deletion of approximately 40 amino acid residues: prelarge contained the sequence of large plus an additional sequence of 25-35 amino acid residues; and presmall contained the sequence of small plus the same additional sequence as in prelarge. The four proteins were also treated with 2-(2-nitrophenylsulfenyl)-3-methyl-3'-bromoindolienine (BNPS-skatole) which cleaves proteins specifically at tryptophan residues. Analysis of the cleavage products indicated that the additional amino acid sequence in both prelarge and presmall extends from the amino terminus of the molecule. Several implications of these results are discussed.

Animals

Construction and characterization of the hybrid bacteriophage lambda Charon vectors for DNA cloning.

Twenty hybrid lambda phages especially designed for molecular cloning have been constructed and named Charon phages. These phages differ in the ranges of sizes of DNA fragments that may be inserted, by the selections and screens which may be used to isolate and detect the incorporation of cloned fragments, by the way transcription of the cloned fragment may be controlled, by the different restriction enzymes that can be used for cloning, by the phage immunities that may be employed for controlling replication and transcription, and by the biological safety features that they contain. The crosses used to produce the vectors are described, and their genealogy is discussed. The structure of each vector has been verified by genetic tests, by DNA length determinations, by electron micrographic analysis of DNA heteroduplexes, and by gel electrophoresis of restriction enzyme digests. In the course of these constructions, a new EcoRI site was found in a derivative of lambda Aam32Bam1 which maps very near the left cohesive end of lambda.

Coliphages

Multiple forms with glucose 6-phosphate dehydrogenase activity in Musca domestica L. as revealed by electrophoresis on cellulose acetate gel.

Single newly emerged males of Musca domestica, WHO strain, usually show five electrophoretic bands of glucose 6-phosphate dehydrogenase (G6PD) activity. Of these five molecular forms, designated with Roman numerals in order from the origin, we have considered the first three: these have been characterized with respect to their substrate and coenzyme specificity and to their sensitivity to some sulfhydryl inhibitors. The data show band III to be G6P specific, nicotinamide adenine dinucleotide phosphate dependent and to be a type I enzyme according to Kamada and Hori's classification. Bands I and II, on the other hand, show wide substrate specificity and low sensitivity to the sulfhydryl inhibitors assayed. In addition, in the absence of an exogenous substrate and in the presence of nicotinamide adenine dinucleotide as a coenzyme, fairly weak bands, which can be ascribed to the so called "nothing dehydrogenase" effect, are seen in the position I and II. Nevertheless, the data reported do not allow a clear definition of the enzymatic type corresponding to bands I and II of G6PD activity.

Animals