Acetylome analyses provide novel insights into the effects of chronic intermittent hypoxia on hippocampus-dependent cognitive impairment.

Introduction: Chronic intermittent hypoxia (CIH) can negatively affect hippocampal function through various molecular mechanisms. Protein acetylation, a frequently occurring modification, plays crucial roles in synaptic plasticity and cognitive processes. However, the global protein acetylation induced by CIH in the hippocampus and its specific effects on hippocampal function and behavior remain poorly understood. Methods: To address this gap, we conducted a study using liquid chromatography-tandem mass spectrometry to analyze the lysine acetylome and proteome of the hippocampus in healthy adult mice exposed to intermittent hypoxia for 4 weeks (as a CIH model) compared to normoxic mice (as a control). Results: We identified and quantified a total of 2,184 lysine acetylation sites in 1,007 proteins. Analysis of these acetylated proteins revealed disturbances primarily in oxidative phosphorylation, the tricarboxylic acid (TCA) cycle, and glycolysis, all of which are localized exclusively to mitochondria. Additionally, we observed significant changes in the abundance of 21 proteins, some of which are known to be associated with cognitive impairments. Discussion: This study helps to elucidate the molecular mechanisms underlying CIH-induced changes in protein acetylation in the hippocampus. By providing valuable insights into the pathophysiological processes associated with CIH and their impacts on hippocampal function, our findings contribute to a better understanding of the consequences of CIH-induced changes in protein acetylation in the hippocampus and the potential role of CIH in cognitive impairment.

Multiplexing of TMT labeling reveals folate-deficient diet-specific proteome changes in NTDs.

Introduction: In the early stage of embryonic development, the neural tube (NT) cannot be closed properly due to some complex factors, including environmental factors, genetic factors, and the relationship between various factors, leading to the occurrence of neural tube defects (NTDs). Methods: In this study, we induced a mouse model of NTDs by feeding mice with a low-folate diet and intraperitoneally injecting them with 1.5 mg/kg methotrexate on E7.5. Fetal mice were achieved at E13.5, and we extracted proteins from brain tissues with trypsin digestion. After enzymatic digestion, peptides were labeled with TMT/iTRAQ and separated in high-performance liquid chromatography (HPLC) for subsequent liquid chromatography tandem mass spectroscopy (LC-MS/MS) analysis. We used gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotation to analyze proteomic changes and analyze the functional enrichment of differentially expressed proteins (DEPs) in the NTD mice tissues. Results: A low-folate-induced mouse model was successfully constructed. Folate was used as a sensitizing agent, and the teratogenicity rate of the NTD fetal mice increased to 36.5% when the concentration of methotrexate was at 1.5 mg/kg. Mass spectrometry was used to identify 6,614 proteins, and among them, 5,656 proteins were quantified. In the following proteomic analysis, GO classification and KEGG pathway enrichment analysis were conducted, and heatmaps were drawn for differentially expressed proteins (DEPs). The main pathways associated with NTDs, such as the Hedgehog, Wnt, p53, and Hippo signaling pathways and the one-carbon pool mediated by folate, can be identified through a protein-protein interaction (PPI) network. It was also found that the regulation of ribosomal proteins, such as RPL13 and RPL14, which are upregulated in NTDs, has a certain impact on neural tube development. Discussion: Our results revealed proteomic changes in the tissues of low-folate-induced NTD mice. Validation showed that ribosomal proteins play a regulatory role during the development of NTDs and provides new ideas for the pathogenesis and preventive measures of NTDs.

Altered dynamic functional and effective connectivity in drug-naive children with Tourette syndrome.

Tourette syndrome (TS) is a developmental neuropsychiatric disorder characterized by repetitive, stereotyped, involuntary tics, the neurological basis of which remains unclear. Although traditional resting-state MRI (rfMRI) studies have identified abnormal static functional connectivity (FC) in patients with TS, dynamic FC (dFC) remains relatively unexplored. The rfMRI data of 54 children with TS and 46 typically developing children (TDC) were analyzed using group independent component analysis to obtain independent components (ICs), and a sliding-window approach to generate dFC matrices. All dFC matrices were clustered into two reoccurring states, the state transition metrics were obtained. We conducted Granger causality and nodal topological analyses to further investigate the brain regions that may play the most important roles in driving whole-brain switching between different states. We found that children with TS spent more time in state 2 (PFDR < 0.001), a state characterized by strong connectivity between ICs, and switched more quickly between states (PFDR = 0.025) than TDC. The default mode network (DMN) may play an important role in abnormal state transitions because the FC that changed the most between the two states was between the DMN and other networks. Additionally, the DMN had increased degree centrality, efficiency and altered causal influence on other networks. Certain alterations related to executive function (r = -0.309, P < 0.05) and tic symptom ratings (r = 0.282; 0.413, P < 0.05) may represent important aspects of the pathophysiology of TS. These findings facilitate our understanding of the neural basis for the clinical presentation of TS.

Intergenerational association of gut microbiota and metabolism with perinatal folate metabolism and neural tube defects.

Disorders of folic acid metabolism during pregnancy lead to fetal neural tube defects (NTDs). However, the mechanisms still require further investigation. Here, we aim to analyze the brain metabolic profiles of 30 NTDs and 30 healthy fetuses. Our results indicated that low-folate diet during early life played a causal role in cerebral metabolism, especially in lipometabolic disturbance, highlighting the importance of folate in modulating brain development and metabolism. Next, we established a mouse model of NTDs. Interestingly, the differential metabolites are mainly involved in glycerophospholipid metabolism and biosynthesis of unsaturated fatty acids both in human and mice fetal brain. Since intestinal microbes could critically regulate neurofunction via the intestinal-brain axis, we further found the abundances of Firmicutes and Bacteroidetes in the gut of pregnant mice were correlated with the abundances of lipid metabolism related metabolites in the fetal brain. This finding probably reflects the intergenerational microbial-metabolism biomarkers of NTDs.

Multi-omics analysis explores the effect of chronic exercise on liver metabolic reprogramming in mice.

Background: The effect of exercise on human metabolism is obvious. However, the effect of chronic exercise on liver metabolism in mice is less well described. Methods: The healthy adult mice running for 6 weeks as exercise model and sedentary mice as control were used to perform transcriptomic, proteomic, acetyl-proteomics, and metabolomics analysis. In addition, correlation analysis between transcriptome and proteome, and proteome and metabolome was conducted as well. Results: In total, 88 mRNAs and 25 proteins were differentially regulated by chronic exercise. In particular, two proteins (Cyp4a10 and Cyp4a14) showed consistent trends (upregulated) at transcription and protein levels. KEGG enrichment analysis indicated that Cyp4a10 and Cyp4a14 are mainly involved in fatty acid degradation, retinol metabolism, arachidonic acid metabolism and PPAR signaling pathway. For acetyl-proteomics analysis, 185 differentially acetylated proteins and 207 differentially acetylated sites were identified. Then, 693 metabolites in positive mode and 537 metabolites in negative mode were identified, which were involved in metabolic pathways such as fatty acid metabolism, citrate cycle and glycolysis/gluconeogenesis. Conclusion: Based on the results of transcriptomic, proteomics, acetyl-proteomics and metabolomics analysis, chronic moderate intensity exercise has certain effects on liver metabolism and protein synthesis in mice. Chronic moderate intensity exercise may participate in liver energy metabolism by influencing the expression of Cyp4a14, Cyp4a10, arachidonic acid and acetyl coenzyme A and regulating fatty acid degradation, arachidonic acid metabolism, fatty acyl metabolism and subsequent acetylation.

Disturbed microbiota-metabolites-immune interaction network is associated with olfactory dysfunction in patients with chronic rhinosinusitis.

Purpose: Olfactory dysfunction (OD) is a debilitating symptom frequently reported by patients with chronic rhinosinusitis (CRS) and it is associated with a dysregulated sinonasal inflammation. However, little information is available about the effect of the inflammation-related nasal microbiota and related metabolites on the olfactory function in these patients. Therefore, the current study aimed to investigate the nasal microbiota-metabolites-immune interactions and their role in the pathogenesis of OD in CRS patients. Methods: 23 and 19 CRS patients with and without OD, respectively, were enrolled in the present study. The "Sniffin' Sticks" was used to measure the olfactory function, while the metagenomic shotgun sequencing and the untargeted metabolite profiling were performed to assess the differences in terms of the nasal microbiome and metabolome between the two groups. The levels of nasal mucus inflammatory mediators were investigated by a multiplex flow Cytometric Bead Array (CBA). Results: A decreased diversity in the nasal microbiome from the OD group compared to the NOD group was evidenced. The metagenomic analysis revealed a significant enrichment of Acinetobacter johnsonii in the OD group, while Mycoplasma arginini, Aeromonas dhakensis, and Salmonella enterica were significantly less represented (LDA value > 3, p < 0.05). The nasal metabolome profiles were significantly different between the OD and NOD groups (P < 0.05). The purine metabolism was the most significantly enriched metabolic subpathway in OD patients compared with NOD patients (P < 0.001). The expressions of IL-5, IL-8, MIP-1α, MCP-1, and TNF were statistically and significantly increased in the OD group (P < 0.05). All these data, including the dysregulation of the nasal microbiota, differential metabolites, and elevated inflammatory mediators in OD patients demonstrated a clear interaction relationship. Conclusion: The disturbed nasal microbiota-metabolite-immune interaction networks may be implicated in the pathogenesis of OD in CRS patients and the underlying pathophysiological mechanisms need to be further investigated in future studies.

Sodium butyrate mediates histone crotonylation and alleviated neonatal rats hypoxic-ischemic brain injury through gut-brain axis.

Neonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats. Surprisingly, Sodium butyrate (SB) treatment could ameliorate pathological damage both in the cerebral cortex and hippocampus and facilitate recovery of SCFAs-producing bacteria related to metabolic pathways in neonatal HIBD rats. Moreover, we found that in samples from SB treatment neonatal HIBD rats cortex with high levels of butyrate acid along with aberrant key crotonyl-CoA-producing enzymes ACADS levels were observed compared HIBD rats. We also demonstrated that a decrease in histone 3-lysine 9-crotonylation (H3K9cr) downregulated expression of the HIE-related neurotrophic genes Bdnf, Gdnf, Cdnf, and Manf in HIBD rats. Furthermore, SB restored H3K9cr binding to HIE-related neurotrophic genes. Collectively, our results indicate that SB contributes to ameliorate pathology of HIBD by altering gut microbiota and brain SCFAs levels subsequently affecting histone crotonylation-mediated neurotrophic-related genes expression. This may be a novel microbiological approach for preventing and treating HIE.

Abnormal transcriptome-wide DNA demethylation induced by folate deficiency causes neural tube defects.

Neural tube defect (NTDs) is one of the most common and serious fetal and neonatal birth defects. Neural tube closure (NTC) is an exquisitely coordinated process and this procedure is influenced by both genetic and environmental factor. Folic acid (FA) supplementation is an effective for prevention of a proportion of NTDs, however, the mechanism remains unclear. In this study, our data demonstrated genome-wide enrichment of 5-hydroxymethylcytosine (5hmC) modification on active transcriptional start sites (TSS) and decreased 5-methylcytosine (5mC) binding to TSS under folate deficiency in mESCs (mouse embryonic stem cells). Furthermore, folate deficiency promoted 5hmC enrichment enhancer histone 3 lysine 27 acetylation (H3K27ac) binding to Shh pathway genes in mESCs. Upregulation of Shh target genes was observed in mouse brain tissue under low levels of maternal serum folate, along with increased expression of 5-methylcytosine dioxygenase Tet1 levels. Taken together, we found that folate deficiency promoted DNA demethylation and enriched 5hmC through recruitment of H3K27ac to activate the Shh signaling pathway. These results suggest that the 5hmC modification increases concomitantly with a positive correlation to Shh gene expression in folate deficiency-induced mouse NTDs.

Quantification of the carbon released by a marine fish using a carbon release model and radiocarbon.

Here we propose a carbon release model that divides fish-released carbon into two sources (ingested food and the fish body), and three forms (dissolved organic carbon (DOC), CO2, and particulate carbon (PC)). We quantified the daily carbon budget of a marine fish Oryzias melastigma by feeding the fish radiocarbon-labeled living rotifer. We found that 91%-92%, 25%-47%, 28%-50%, 20%-31%, and 8%-9% of the ingested food carbon was absorbed, assimilated, and released as DOC, CO2, and PC, respectively. Fish body carbon dissimilated/catabolized and released as 0.053-0.12 d-1 at two daily food rations. DOC, CO2, and PC accounted for 39%-42%, 39%-45%, and 16%-19% of the released fish body carbon, respectively. Our study shows that the fish transformed substantial fractions of their daily ingested food and dissimilated body carbon into DOC, and fish may be an important source of DOC in the ocean.

The Alternation of Gray Matter Morphological Topology in Drug-Naïve Tourette's Syndrome in Children.

Tourette syndrome (TS) is a neurodevelopment disorder characterized by motor and phonic tics. We investigated the topological alterations in pediatric TS using morphological topological analysis of brain structures. We obtained three-dimensional T1-weighted magnetic resonance imaging (MRI) sequences from 59 drug-naïve pediatric patients with TS and 87 healthy controls. We identified morphological topographical alterations in the brains of patients with TS compared to those of the healthy controls via GRETNA software. At the global level, patients with TS exhibited increased global efficiency (E glob ) (p = 0.012) and decreased normalized characteristic path length (λ) (p = 0.027), and characteristic path length (Lp) (p = 0.025) compared to healthy controls. At the nodal level, we detected significant changes in the nodal betweenness, nodal degree, and nodal efficiency in the cerebral cortex-striatum-thalamus-cortex circuit. These changes mainly involved the bilateral caudate nucleus, left thalamus, and gyri related to tics. Nodal betweenness, nodal degree, and nodal efficiency in the right superior parietal gyrus were negatively correlated with the motor tic scores of the Yale Global Tic Severity Scale (YGTSS) (r = -0.328, p = 0.011; r = -0.310, p = 0.017; and r = -0.291, and p = 0.025, respectively). In contrast, nodal betweenness, nodal degree, and nodal efficiency in the right posterior cingulate gyrus were positively correlated with the YGTSS phonic tic scores (r = 0.353, p = 0.006; r = 0.300, p = 0.021; r = 0.290, and p = 0.026, respectively). Nodal betweenness in the right supplementary motor area was positively correlated with the YGTSS phonic tic scores (r = 0.348, p = 0.007). The nodal degree in the right supplementary motor area was positively correlated with the YGTSS phonic tic scores (r = 0.259, p = 0.048). Diagnosis by age interactions did not display a significant effect on brain network properties at either the global or nodal level. Overall, our findings showed alterations in the gray matter morphological networks in drug-naïve children with TS. These findings enhance our understanding of the structural topology of the brain in patients with TS and provide useful clues for exploring imaging biomarkers of TS.

Folate-deficiency induced acyl-CoA synthetase short-chain family member 2 increases lysine crotonylome involved in neural tube defects.

Maternal folate deficiency increases the risk of neural tube defects (NTDs), but the mechanism remains unclear. Here, we established a mouse model of NTDs via low folate diets combined with MTX-induced conditions. We found that a significant increase in butyrate acid was observed in mouse NTDs brains. In addition, aberrant key crotonyl-CoA-producing enzymes acyl-CoA synthetase short-chain family member 2 (ACSS2) levels and lysine crotonylation (Kcr) were elevated high in corresponding low folate content maternal serum samples from mouse NTD model. Next, proteomic analysis revealed that folate deficiency led to global proteomic modulation, especially in key crotonyl-CoA-producing enzymes, and dramatic ultrastructural changes in mouse embryonic stem cells (mESCs). Furthermore, we determined that folate deficiency induced ACSS2 and Kcr in mESCs. Surprisingly, folic acid supplementation restored level of ACSS2 and Kcr. We also investigated overall protein post-translational Kcr under folate deficiency, revealing the key regulation of Kcr in glycolysis/gluconeogenesis, and the citric acid cycle. Our findings suggest folate deficiency leads to the occurrence of NTDs by altering ACSS2. Protein crotonylation may be the molecular basis for NTDs remodeling by folate deficiency.

Physiological and behavioral responses of the copepod Temora turbinata to hypoxia.

Hypoxia is intensified in tropical and subtropical estuarine and coastal waters and brings about lethal and sublethal effects to marine copepods. The physiological and behavioral responses of the subtropical calanoid copepod Temora turbinata were tested after short-term exposure to hypoxia. The LD50 values were 3.02 ± 0.21, 2.00 ± 0.35, and 3.11 ± 0.31 mg L-1 for nauplii (II-III), copepodites (II-III), and female adults, respectively. With a decrease in the ambient dissolved oxygen (DO) level from 8 to 0.5 mg L-1, the ingestion rates decreased significantly at all life stages, as did oxygen consumption in female adults. In an artificial stratification column with a DO gradient, female adults exhibited an obvious avoidance response to the hypoxic bottom layer. Our study provides preliminary evidence for high hypoxia sensitivity in T. turbinata and implies that the DO level may be the main factor controlling the distribution of this species in tropical and subtropical coastal and estuarine waters.

Down-regulation of long noncoding RNA LINC00472 alleviates sepsis-induced acute hepatic injury by regulating miR-373-3p/TRIM8 axis.

BACKGROUND: The long noncoding RNAs (lncRNAs) have been confirmed to be involved in sepsis-induced organ injury. Here, we first investigated the functional role and the underlying mechanism of lncRNA LINC00472 in sepsis-induced acute hepatic injury (AHI). METHODS: Human liver THLE-3 cells were treated with lipopolysaccharide (LPS) to mimic sepsis-induced AHI in vitro; intraperitoneal injection of LPS in rats were used as an in vivo model of AHI induced by sepsis. The expressions of LINC00472, miR-373-3p, and TRIM8 mRNA were detected by qRT-PCR. The effects of LINC00472 and miR-373-3p on the viability of THLE-3 cells were assessed by CCK-8 assay. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to determine the binding relationship between LINC00472 and miR-373-3p as well as between miR-373-3p and TRIM8. The expressions of apoptosis-related proteins and TRIM8 were detected by Western blot; the levels of ALT, AST, TNF-α, IL-6, and IL-10 in the serum of rats were measured using ELSA assay. RESULTS: LINC00472 and TRIM8 were significantly upregulated in liver tissues and THLE-3 cells in sepsis-induced AHI models, while miR-373-3p was downregulated. Silencing of LINC00472 promoted cell viability and suppressed cell apoptosis in LPS-treated THLE-3 cells, whereas upregulation of LINC00472 had the opposite effect. Moreover, LINC00472 served as a sponge for miR-373-3p and negatively regulated its expression. miR-373-3p mimics could promote THLE-3 cell viability and suppress cell apoptosis. Additionally, TRIM8 was a direct target of miR-373-3p, which was downregulated in LINC00472-silenced cells and upregulated by the miR-373-3p inhibitor. Further, the co-transfection of miR-373-3p inhibitor reversed the effects of LINC00472 knockdown on cell viability and apoptosis. Downregulation of LINC00472 in rats restored the levels of ALT, AST, IL-6, IL-10, and TNF-α. CONCLUSION: Downregulation of LINC00472 ameliorates sepsis-induced AHI by regulating the miR-373-3p/TRIM8 axis.

Allocation and stoichiometric regulation of phosphorus in a freshwater zooplankton under limited conditions: Implication for nutrient cycling.

Because zooplankton is potentially limited by phosphorus (P) in freshwater, they may modify their body P distributions in different biochemical and anatomic components depending on the environmental P levels. In the present study, we quantified the distribution and regulation of P in a freshwater zooplankton Daphnia magna under P-limited conditions by using 33P as a radiotracer. We demonstrated that the P allocation patterns in D. magna were independent of the ontogenic development. Carapace accounted for 35-54% of total body P, followed by small molecules and nucleic acids (11-30%), whereas phospholipids represented only a minor P pool. The proportion of body P allocated into carapace decreased from 51.8% in +P adults to 16.5% in the -P adults, and a lower proportion of body P was also allocated to eggs in the -P adults than in the +P adults (3.8 vs. 16.5%). Meanwhile, no difference in allocation pattern was detected in the juveniles under +P and -P conditions, demonstrating an interaction between effects of P condition and ontogeny. Furthermore, the P turnover rates of nucleic acids and phospholipids in the -P juveniles were only half of those found in the +P individuals, suggesting a reduced metabolic rate under P-deficient conditions. However, the P turnover rate of small molecules, nucleic acids and phospholipids did not vary with the P condition in adults. It appeared that the adults could maintain their basic P metabolism by down-regulating the P allocation to carapace and eggs. Our results provide an insight into the tolerance of zooplankton to P-deficiency and bear implications on involvement of Daphnia in regulation of P cycling and availability in the epilimnion.

Influence of Hydrological Heterogeneity on Rotifer Community Structure in Three Different Water Bodies in Shantou Area, Guangdong (China).

Rotifers, small but essential invertebrates in aquatic ecosystems, are sensitive to environmental changes and are proposed to be indicators of trophic state. However, the effects of hydrological heterogeneity on the rotifer community and the ability of rotifer indices to reflect trophic state across different water bodies are still unclear. Here, we investigated rotifer community structure in different seasons in the three types of water bodies: Han river downstream (HD), Reservoir (RE) and Tidal creek (TC) in Shantou City, Guangdong, China. Our findings revealed that rotifer community structure differes significantly among the three water bodies, resulting from a dominance of Keratella cochlearis, Anuraeopsis fissa and Polyarthra vulgaris, who largely accounted for the differences in water bodies. Chlorophyll-a and transparency were the main environmental drivers in RE rotifer communities, while total nitrogen, total phosphorus and salinity were the main factors in HD and TC communities. Rotifer abundance and the rotifer trophic state index decreased in the order: RE > HD > TC. However, both the Sladecek's B/T quotient and the Keratella- index decreased in the order: HD > RE > TC, which was in accordance with the Carlson's trophic index. We conclude that it is efficient to use rotifer composition in water quality assessments when comparing different water bodies. Alpha diversity of rotifers was the highest in HD, which is consistent with the intermediate disturbance hypothesis. Hydrological heterogeneity is the micro-factor that regulates rotifer community structures in the Shantou area.

Allocation Costs Associated with Induced Defense in Phaeocystis globosa (Prymnesiophyceae): the Effects of Nutrient Availability.

Colony enlargement in Phaeocystis globosa has been considered as an induced defense strategy that reduces its susceptibility to grazers, but allocation costs inflicted by this plastic morphological defense are poorly understood. We conducted experiments in which P. globosa cultures were exposed to chemical cues from copepods, ciliates and heterotrophic dinoflagellates, respectively, under nutrient sufficient and deficient conditions to evaluate allocation costs associated with induced defense. Phaeocystis globosa responded to chemical cues from grazers by increasing colony diameter irrespective of nutrient conditions. We did not find trade-offs between induced defense and growth rate under nutrient sufficient conditions. Instead, induced defensive P. globosa had higher growth rates than non-induced P. globosa. When nutrient became limited, P. globosa exposed to grazing cues from copepods and dinoflagellates had significantly decreased growth rates when compared with non-induced P. globosa. We suggested that the decreased growth revealed allocation costs associated with induced defense that may influence on the trophic interactions between Phaeocystis and consumers.

[Algae identification research based on fluorescence spectral imaging technology combined with cluster analysis and principal component analysis].

In order to explore rapid real-time algae detection methods, in the present study experiments were carried out to use fluorescence spectral imaging technology combined with a pattern recognition method for identification research of different types of algae. The fluorescence effect of algae samples is obvious during the detection. The fluorescence spectral imaging system was adopted to collect spectral images of 40 algal samples. Through image denoising, binarization processing and making sure the effective pixels, the spectral curves of each sample were drawn according to the spectral cube. The spectra in the 400-720 nm wavelength range were obtained. Then, two pattern recognition methods, i.e., hierarchical cluster analysis and principal component analysis, were used to process the spectral data. The hierarchical cluster analysis results showed that the Euclidean distance method and average weighted method were used to calculate the cluster distance between samples, and the samples could be correctly classified at a level of the distance L=2.452 or above, with an accuracy of 100%. The principal component analysis results showed that first-order derivative, second-order derivative, multiplicative scatter correction, standard normal variate and other pretreatments were carried out on raw spectral data, then principal component analysis was conducted, among which the identification effect after the second-order derivative pretreatment was shown to be the most effective, and eight types of algae samples were independently distributed in the principal component eigenspace. It was thus shown that it was feasible to use fluorescence spectral imaging technology combined with cluster analysis and principal component analysis for algae identification. The method had the characteristics of being easy to operate, fast and nondestructive.