Magnetic resonance imaging-based prediction models for differentiating intraspinal schwannomas from meningiomas: classification and regression tree and random forest analysis.

Background: Due to the variations in surgical approaches and prognosis between intraspinal schwannomas and meningiomas, it is crucial to accurately differentiate between the two prior to surgery. Currently, there is limited research exploring the implementation of machine learning (ML) methods for distinguishing between these two types of tumors. This study aimed to establish a classification and regression tree (CART) model and a random forest (RF) model for distinguishing schwannomas from meningiomas. Methods: We retrospectively collected 88 schwannomas (52 males and 36 females) and 51 meningiomas (10 males and 41 females) who underwent magnetic resonance imaging (MRI) examinations prior to the surgery. Simple clinical data and MRI imaging features, including age, sex, tumor location and size, T1-weighted images (T1WI) and T2-weighted images (T2WI) signal characteristics, degree and pattern of enhancement, dural tail sign, ginkgo leaf sign, and intervertebral foramen widening (IFW), were reviewed. Finally, a CART model and RF model were established based on the aforementioned features to evaluate their effectiveness in differentiating between the two types of tumors. Meanwhile, we also compared the performance of the ML models to the radiologists. The receiver operating characteristic (ROC) curve, accuracy, sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were used to evaluate the models and clinicians' discrimination performance. Results: Our investigation reveals significant variations in ten out of 11 variables in the training group and five out of 11 variables in the test group when comparing schwannomas and meningiomas (P<0.05). Ultimately, the CART model incorporated five variables: enhancement pattern, the presence of IFW, tumor location, maximum diameter, and T2WI signal intensity (SI). The RF model combined all 11 variables. The CART model, RF model, radiologist 1, and radiologist 2 achieved an area under the curve (AUC) of 0.890, 0.956, 0.681, and 0.723 in the training group, and 0.838, 0.922, 0.580, and 0.659 in the test group, respectively. Conclusions: The RF prediction model exhibits more exceptional performance than an experienced radiologist in discriminating intraspinal schwannomas from meningiomas. The RF model seems to be better in discriminating the two tumors than the CART model.

The existence of ferric hydroxide links the carbon and nitrogen cycles by promoting nitrite-coupled methane anaerobic oxidation.

Microorganism-mediated anaerobic oxidation of methane can efficiently mitigate methane atmospheric emissions and is a key process linking the biogeochemical cycles of carbon, nitrogen, and iron. The results showed that methane oxidation and nitrite removal rates in the CF were 1.12 and 1.28 times higher than those in CK, respectively, suggesting that ferric hydroxide can enhance nitrite-driven AOM. The biochemical process was mediated by the enrichment of methanogens, methanotrophs, and denitrifiers. Methanobacterium and Methanosarcina were positively correlated with Fe3+ and Fe2+, whereas Methylocystis and Methylocaldum were positively correlated with methane, and denitrifiers were positively correlated with nitrite. Metagenomic analysis revealed that the genes related to methane oxidation, nitrogen reduction, and heme c-type cytochrome were upregulated in CF, indicating that a synergistic action of bacteria and methanogens drove AOM via diverse metabolic pathways, within which ferric hydroxide played a crucial role. This study provides novel insights into the synergistic mechanism of ferric iron and nitrite-driven AOM.

Metabolic Mechanism of Bacillus sp. LM24 under Abamectin Stress.

Abamectin (ABM) has been recently widely used in aquaculture. However, few studies have examined its metabolic mechanism and ecotoxicity in microorganisms. This study investigated the molecular metabolic mechanism and ecotoxicity of Bacillus sp. LM24 (B. sp LM24) under ABM stress using intracellular metabolomics. The differential metabolites most affected by the bacteria were lipids and lipid metabolites. The main significant metabolic pathways of B. sp LM24 in response to ABM stress were glycerolipid; glycine, serine, and threonine; and glycerophospholipid, and sphingolipid. The bacteria improved cell membrane fluidity and maintained cellular activity by enhancing the interconversion pathway of certain phospholipids and sn-3-phosphoglycerol. It obtained more extracellular oxygen and nutrients to adjust the lipid metabolism pathway, mitigate the impact of sugar metabolism, produce acetyl coenzyme A to enter the tricarboxylic acid (TCA) cycle, maintain sufficient anabolic energy, and use some amino acid precursors produced during the TCA cycle to express ABM efflux protein and degradative enzymes. It produced antioxidants, including hydroxyanigorufone, D-erythroascorbic acid 1'-a-D-xylopyranoside, and 3-methylcyclopentadecanone, to alleviate ABM-induced cellular and oxidative damage. However, prolonged stress can cause metabolic disturbances in the metabolic pathways of glycine, serine, threonine, and sphingolipid; reduce acetylcholine production; and increase quinolinic acid synthesis.

Biodegradation of petroleum hydrocarbons based pollutants in contaminated soil by exogenous effective microorganisms and indigenous microbiome.

Microbial remediation is an eco-friendly and promising approach for the restoration of sites contaminated by petroleum hydrocarbons (PHCs). The degradation of total petroleum hydrocarbons (TPHs), semi volatile organic compounds (SVOCs) and volatile organic compounds (VOCs) of the soil samples collected from a petrochemical site by indigenous microbiome and exogenous microbes (Saccharomyces cerevisiae ATCC 204508/S288c, Candida utilis AS2.281, Rhodotorula benthica CBS9124, Lactobacillus plantarum S1L6, Bacillus thuringiensis GDMCC1.817) was evaluated. Community structure and function of soil microbiome and the mechanism involved in degradation were also revealed. After bioremediation for two weeks, the concentration of TPHs in soil samples was reduced from 17,800 to 13,100 mg/kg. The biodegradation efficiencies of naphthalene, benzo[a]anthracene, benzo[b]fluoranthene, benzo[a]pyrene, indeno[1,2,3-cd]pyrene, dibenzo[a,h]anthracene, 1,2,3-trichloropropane, 1,2-dichloropropane, ethylbenzene and benzene in soil samples with the addition of S. cerevisiae were 38.0%, 35.7%, 36.2%, 40.4%, 33.6%, 36.2%, 12.0%, 43.9%, 43.3% and 43.0%, respectively. The microbial diversity and community structure were improved during the biodegradation process. S. cerevisiae supplemented soil samples exhibited the highest relative abundance of the genus Acinetobacter for bacteria and Saccharomyces for yeast. The findings offer insight into the correlation between microbes and the degradation of PHC-based pollutants during the bioremediation process.

Triclocarban triggers osteoarthritis via DNMT1-mediated epigenetic modification and suppression of COL2A in cartilage tissues.

Triclocarban (TCC) is a widely used environmental endocrine-disrupting chemical (EDC). Articular injury of EDCs has been reported; however, whether and how TCCs damage the joint have not yet been determined. Herein, we revealed that exposure to TCC caused osteoarthritis (OA) within the zebrafish anal fin. Mechanistically, TCC stimulates the expression of DNMT1 and initiates DNA hypermethylation of the type II collagen coding gene, which further suppresses the expression of type II collagen and other extracellular matrices. This further results in decreased cartilage tissue and narrowing of the intraarticular space, which is typical of the pathogenesis of OA. The regulation of OA occurrence by TCC is conserved between zebrafish cartilage tissue and human chondrocytes. Our findings clarified the hazard and potential mechanisms of TCC towards articular health and highlighted DNMT1 as a potential therapeutic target for OA caused by TCC.

The synergy of Fe(III) and NO2- drives the anaerobic oxidation of methane.

The anaerobic oxidation of methane (AOM) driven by NO2- or Fe(III) alone was limited by slow electron delivery and ineffective enrichment of microbes. The flexible coupling between Fe(III) and NO2- potentially cooperated to accelerate AOM. One negative control was fed CH4 and NO2-, and four treatment reactors were supplemented with CH4, NO2- and ferric citrate (FC)/ferric chloride (FCH)/ chelate iron (FCI)/ferric hydroxide (FH) and were anaerobically operated for 1200 days to verify the synergy and promicrobial roles of Fe(III) and NO2- in improving AOM. The changes in gas and ion profiles were observed in the reactors, and microbial development was studied using 16S rRNA gene sequencing with the Illumina platform. The results indicated that the combined Fe(III) and NO2- treatment improved AOM, and their synergy followed the order of FC > FCI > FCH > FH. The biochemical reaction of Fe3+ with NO2- and its secondary process accelerated electron transfer to microbial cells and subsequently enhanced AOM in the reactors. The total organic carbon (TOC) content, NH4+ content, NO3- content, and pH value altered the dominant bacteria the most in the FC reactor, FCI, FCH, and FH groups, respectively. Several dominant bacterial species were enriched, whereas only two archaea were highly concentrated in the FC and FCI groups. Only bacteria were detected in the FCH group, and archaea contributed substantially to the FH group. These findings contribute to an improved understanding of the interactions among nitrogen, iron and CH4 that are paramount to accelerating the process of AOM for engineering applications.

Disrupted metabolic pathways and potential human diseases induced by bisphenol S.

Although the toxicity of bisphenol S has been studied in some species, the global metabolic network disrupted by bisphenol S remains unclear. To this end, published datasets related to the genes, proteins, and metabolites disturbed by bisphenol S were investigated through omics methods. The dataset revealed that bisphenol S at high concentrations tended to downregulate biomolecules, while low concentrations of bisphenol S tended to enhance metabolic reactions. The results showed that exposure to bisphenol S upregulated estrogen and downregulated androgen metabolism in humans, mice, rats, and zebrafish. Fatty acid metabolism and phospholipid metabolism in mice were upregulated. Reactions in amino acid metabolism were upregulated, with the exception of the suppressive conversion of arginine to ornithine. In zebrafish, fatty acid synthesis was promoted, while nucleotide metabolism was primarily depressed through the downregulation of pyruvate 2-o-phosphotransferase. The interference in amino acid metabolism by bisphenol S could trigger Alzheimer's disease, while its disturbance of glucose metabolism was associated with type II diabetes. Disturbed glycolipid metabolism and vitamin metabolism could induce Alzheimer's disease and diabetes. These findings based on omics data provide scientific insight into the metabolic network regulated by bisphenol S and the diseases triggered by its metabolic disruption.

Novel perspectives of environmental proteomics.

The connection among genome expression, proteome alteration, metabolism regulation and phenotype change under environmental stresses is very vague. It is a tough task for the traditional research approaches to reveal the related scientific mechanisms of the above connection at molecular and systematic levels. Proteomics approach is an insightful tool for revealing the biological functions, metabolic networks and functional protein interaction networks of cells and organisms under stresses at the systematic level. The purpose of this review is to provide an insightful guideline on how to set up a proteomic investigation for revealing biomolecule mechanisms, protein biomarkers and metabolism networks related to stress response, pollutant recognition, transport and biodegradation, and providing an insightful high-throughput approach for screening functional enzymes and effective microbes based on bioinformatics and functional verification method. Furthermore, the toxicity evaluation of pollutants and byproducts by proteomics approaches provides a scientific insight for early diagnosis of ecological risk and determination of the effectiveness of pollutant treatment techniques.

Proteome of Saccharomyces cerevisiae under paraquat stress regulated by therapeutic concentration of copper ions.

Paraquat (PQ) is a non-selective herbicide with strong toxicity to humans and mammals. However, the proteome regulation of cells by PQ is still unclear, limiting the development of effective antidotes. Studies have shown that a slight excess of intracellular copper levels could be beneficial to the survival under exposure to PQ. In this study, Saccharomyces cerevisiae was used as a model to explore the regulation effect of copper ions on PQ poisoning by the approach of date independent acquisition proteomics. The results showed that toxic effect of PQ was primarily induced by oxidative damage in the mitochondria and the disorder of gene expression. The addition of Cu2+ involved a series of favorable reactions to cell survival under PQ stress, including activation of the mitogen-activated protein kinase signaling pathway, regulation of processes such as sulfur metabolism, carbon metabolism and gene expression in cells. The generation of glutathione, heme and steroids advantageous to cell growth under stress was also increased. These findings inferred that therapeutic concentration of copper ions could prolong the survival of cells under PQ stress.

Comparative toxicity reduction potential of UV/sodium percarbonate and UV/hydrogen peroxide treatments for bisphenol A in water: An integrated analysis using chemical, computational, biological, and metabolomic approaches.

Bisphenol A (BPA) is a common industrial chemical with significant adverse impacts on biological systems as an environmental contaminant. UV/hydrogen peroxide (UV/H2O2) is a well-established technology for BPA treatment in water while UV/sodium percarbonate (UV/SPC) is an emerging technology with unclear biological impacts of treated effluent. Therefore, in this study, the toxicity evaluation of BPA solution treated with UV/H2O2 and UV/SPC was preformed and compared based on transformation products (TPs) profile, quantitative structure-activity relationship (QSAR), Escherichia coli (E. coli) toxicity assays, and metabolomic analysis. TPs with hydroxylation, double-ring split, and single-ring cleavage were generated from BPA during the treatments with both technologies, but TPs with quinonation were specifically detected in UV/H2O2 treated solution at the UV dose of 1470 mJ cm-2. QSAR prediction based on TPs profile (excluding benzoquinone TPs) suggested that UV/H2O2 and UV/SPC treatments of BPA may increase matrix toxicity due to the formation of multi-hydroxylated TPs; however decreased bioaccumulation potential of all TPs may mitigate the increase of toxicity by reducing the chance of TPs to reach the concentration of toxicity threshold. In vivo assays with E. coli showed inhibited cell growth, arrested cell cycle, and increased cell death in BPA solution treated with UV/H2O2 at the UV dose of 1470 mJ cm-2. Metabolomic analysis indicated that BPA solution treated with UV/H2O2 at UV dose of 1470 mJ cm-2 impacted E. coli metabolism differently than other solutions with unique inhibition on glycerolipid metabolism. Moreover, BPA interfered in various metabolic pathways including alanine, aspartate and glutamate metabolism, starch and sucrose metabolism, pentose phosphate pathway, and lysine degradation, which were mitigated after the treatments. UV/SPC showed advantage over UV/H2O2 of attenuated impact on butanoate metabolism with UV irradiation. This study has generated valuable data for better understanding of biological impacts of BPA and its solutions treated with UV/H2O2 or UV/SPC, thus providing insights for their application prospect for water and wastewater treatment.

Deltamethrin transformation by Bacillus thuringiensis and the associated metabolic pathways.

The biological toxicity of deltamethrin at molecular level has been investigated, whereas, the proteome responsive mechanisms of cells under deltamethrin stress at the phylogenetic level are not clear. The proteome expression, transformation-related pathway and regulatory network of Bacillus thuringiensis during the process of deltamethrin transformation were explored using proteomics and metabolomics approaches in the present study. The results showed that deltamethrin was effectively removed by B. thuringiensis within 48 h. The stress responses of B. thuringiensis were activated to resist deltamethrin stress, with significant differential expression of proteins that were primarily involved in the synthesis of DNA and shock proteins, endospore formation, carbon metabolism. The expression patterns of ribosomal proteins confirmed that the transcription and translation of DNA, and biosynthesis of heat shock proteins were inhibited as deltamethrin transformation. The synthesis of oxaloacetate and acetyl-CoA were also hindered, resulting in downregulated expression of carbohydrate metabolism, TCA cycle and energy metabolism. Meanwhile, endospore formation and germination were promoted to resist oxidative stress induced by deltamethrin. These findings imparted novel insight to elucidate underlying stress response mechanisms of the organism under target contaminants stress, and the interaction between deltamethrin transformation and cellular metabolism at the pathway and network levels.

Circulating metabolomics profiling reveals novel pathways associated with cognitive decline in patients with hypertension.

BACKGROUND: Hypertension is a significant risk factor for cardiovascular disease, and it is associated with dementia, including Alzheimer's disease (AD). Although it may be correlated with AD in terms of symptoms, the link between hypertension and AD pathological biomarkers, and the potential underlying mechanism of hypertension with cognitive decline, are still not well understood. METHODS: The Mini-Mental State Examination (MMSE) scores were used to evaluate cognitive function. Enzyme-linked immunosorbent assays were used to examine plasma amyloid-beta (Aß)40, Aß42, and tau concentration in hypertensive patients. Metabolomics and metagenomics were performed to identify the significantly changed circulating metabolites and microbiota between healthy individuals and hypertensive patients. Pearson's correlation was used to examine the association between cognitive indicators and differential metabolites. RESULTS: We found significantly decreased MMSE scores, elevated plasma Aß40, and decreased Aß42/Aß40 ratio in hypertensive patients, which are critically associated with AD pathology. Based on metabolomics, we found that significantly altered metabolites in the plasma of hypertensive patients were enriched in the benzoate degradation and phenylpropanoid biosynthesis pathways, and they were also correlated with changes in MMSE scores and Aß42/Aß40 ratio. In addition, metabolomics signaling pathway analysis suggested that microbial metabolism was altered in hypertensive patients. We also identified altered blood microbiota in hypertensive patients compared with the controls. CONCLUSIONS: Our study provides a novel metabolic and microbial mechanism, which may underlie the cognitive impairment in hypertensive patients.

Metabolic network and recovery mechanism of Escherichia coli associated with triclocarban stress.

Although the toxicity of triclocarban at molecular level has been investigated, the metabolic networks involved in regulating the stress processes are not clear. Whether the cells would maintain specific phenotypic characteristics after triclocarban stress is also needed to be clarified. In this study, Escherichia coli was selected as a model to elucidate the cellular metabolism response associated with triclocarban stress and the recovery metabolic network of the triclocarban-treated cells using the proteomics and metabolomics approaches. Results showed that triclocarban caused systematic metabolic remodeling. The adaptive pathways, glyoxylate shunt and acetate-switch were activated. These arrangements allowed cells to use more acetyl-CoA and to reduce carbon atom loss. The upregulation of NH3-dependent NAD+ synthetase complemented the NAD+ consumption by catabolism, maintaining the redox balance. The synthesis of 1-deoxy-D-xylulose-5-phosphate was suppressed, which would affect the accumulation of end products of its downstream pathway of isoprenoid synthesis. After recovery culture for 12 h, the state of cells returned to stability and the main impacts on metabolic network triggered by triclocarban have disappeared. However, drug resistance caused by long-term exposure to environmentally relevant concentration of triclocarban is still worthy of attention. The present study revealed the molecular events under triclocarban stress and clarified how triclocarban influence the metabolic networks.

Discovering the Importance of ClO• in a Coupled Electrochemical System for the Simultaneous Removal of Carbon and Nitrogen from Secondary Coking Wastewater Effluent.

Inorganic constituents in real wastewater, such as halides and carbonates/bicarbonates, may have negative effects on the performance of electrochemical systems because of their capability of quenching HO•. However, we discovered that the presence of Cl- and HCO3- in an electrochemical system is conducive to the formation of ClO•, which plays an important role in promoting the simultaneous elimination of biorefractory organics and nitrogen in secondary coking wastewater effluent. The 6-h operation of the coupled electrochemical system (an undivided electrolytic cell with a PbO2/Ti anode and a Cu/Zn cathode) at a current density of 37.5 mA cm-2 allowed the removal of 87.8% of chemical oxygen demand (COD) and 86.5% of total nitrogen. The electron paramagnetic resonance results suggested the formation of ClO• in the system, and the probe experiments confirmed the predominance of ClO•, whose steady-state concentrations (8.08 × 10-13 M) were 16.4, 26.5, and 1609.5 times those of Cl2•- (4.92 × 10-14 M), HO• (3.05 × 10-14 M), and Cl• (5.02 × 10-16 M), respectively. The rate constant of COD removal and the Faradaic efficiency of anodic oxidation obtained with Cl- and HCO3- was linearly proportional to the natural logarithm of the ClO• concentration, and the specific energy consumption was inversely correlated to it, demonstrating the crucial role of ClO• in pollutant removal.

The molecular effects of ultrasound on the expression of cellular proteome.

High frequency and low intensity, diagnostic ultrasound methods are recognized to be safe in epidemiology and pathology but the bioeffects of these methods on molecular and proteomic levels are unknown. As a representative organism that can directly reflect the molecular response to stresses, Escherichia coli was selected for exposure to ultrasound probes C1-5, M5s and 9 L for 10 min and 20 min. ITRAQ was used to measure the expression of the cellular proteome. The results showed that both the frequency and time of exposure to ultrasound affected the proteome expression. Fifty biological processes were affected and nineteen metabolic processes, including carbohydrate metabolism, asparagine metabolism and phosphate import were differentially regulated. Lower frequency ultrasound caused copper export and iron­sulfur cluster biosynthesis upregulation. Nine proteins (GlpD, AsnB, TdcB, CopA, IscR, IscU, IscS, IscA, RecA) were key for the adaption to ultrasound. Accordingly, the results of the potential risks based on the calculation of the orthologous genome clarified that relevant pathways and potentially sensitive individuals were worthy of further study. These findings offer insights into reveal the bioeffects of ultrasound at the metabolic network and proteomic levels.

A cyclic peptide retards the proliferation of DU145 prostate cancer cells in vitro and in vivo through inhibition of FGFR2.

In malignancies, fibroblast growth factor receptors (FGFRs) signaling is reinforced through overexpression of fibroblast growth factors (FGFs) or their receptors. FGFR2 has been proposed as a target for cancer therapy, because both the expression and activation of FGFR2 are boosted in various malignant carcinomas. Although several chemicals have been designed against FGFR2, they did not exhibit enough specificity and might bring potential accumulated toxicity. In this study, we developed an epitope peptide (P5) and its cyclic derivative (DcP5) based on the structure of FGF2 to limit the activation of FGFR2. The anticancer activities of P5 and DcP5 were examined in vitro and in vivo. Our results demonstrated that P5 significantly inhibited the cell proliferation in FGFR2-dependent manner in DU145 cells and retarded tumor growth in DU145 xenograft model with negligible toxicity toward normal organs. Further investigations found that the Gln4 and Glu6 residues of P5 bind to FGFR2 to abolish its activation. Moreover, we developed the P5 cyclic derivative, DcP5, which achieved reinforced stability and anticancer activity in vivo. Our findings suggest P5 and its cyclic derivative DcP5 as potential candidates for anticancer therapy.

Bisphenol A degradation pathway and associated metabolic networks in Escherichia coli harboring the gene encoding CYP450.

Although bisphenol A (BPA) can be transformed by CYP450, the metabolic networks involved in regulating the transformation processes are not clear. In this study, Escherichia coli harboring the gene encoding CYP450 was used as a model to elucidate the BPA degradation pathway and the associated metabolic network using a proteomic approach. The results showed that CYP450 promotes the transformation of BPA, generating 1,2-bis(4-hydroxyphenyl)-2-propanol and 2,2-bis(4-hydroxyphenyl)-1-propanol, with hydroquinone and 4-(2-hydroxypropan-2-yl)phenol formed in another pathway. The DNA adducts formed by 1,4-benzoquinone were reduced, and CYP450 played a positive role in cellular homeostasis by promoting the transformation of BPA and mismatch repair. An increase in the synthesis of cell membrane lipids was observed after dislodging BPA. BPA disturbed folate metabolism by decreasing the abundance of dihydrofolate reductase, which inhibited microbial metabolism in the absence of CYP450. The findings of this study revealed the molecular mechanism associated with the metabolic network responsible for pollutant tolerance and degradation.

Molecular response mechanism in Escherichia coli under hexabromocyclododecane stress.

The effects of hexabromocyclododecane (HBCD) on the relationship between physiological responses and metabolic networks remains unclear. To this end, cellular growth, apoptosis, reactive oxygen species, exometabolites and the proteome of Escherichia coli were investigated following exposure to 0.1 and 1 µM HBCD. The results showed that although there were no significant changes in the pH value, apoptosis and reactive oxygen species under HBCD stress, cell growth was inhibited. The metabolic network formed by glycolysis, oxidative phosphorylation, amino acids biosynthesis, membrane proteins biosynthesis, ABC transporters, glycogen storage, cell recognition, compound transport and nucleotide excision repair was disrupted. Cell chemotaxis and DNA damage repair were the effective approaches to alleviate HBCD stress. This work improves our understanding of HBCD toxicity and provides insight into the toxicological mechanism of HBCD at the molecular and network levels.

Systematic stress adaptation of Bacillus subtilis to tetracycline exposure.

To alleviate the harmful effects of antibiotics on the environment and human health, the stress response and molecular network of Bacillus under tetracycline stress were investigated using a proteomics approach. During the exposure process, Bacillus subtilis exhibited a strong adaptation mechanism. Cell membrane and intracellular reactive oxygen species (ROS) level returned to normal after 5 h. A total of 312 upregulated and 65 downregulated proteins were identified, mainly involved in metabolism and the synthesis of ribosomes, DNA, and RNA. After tetracycline exposure, the core metabolism network was accelerated to supply precursors for the synthesis of DNA, RNA, proteins, peptidoglycans, and saturated fatty acids that were involved in ribosome protection, and strengthened the cell wall and cell membrane. The signal transduction pathways involved were analyzed in association with the stress response of B. subtilis at 15 min of exposure to tetracycline. The primary damage to the ribosome by tetracycline activated a series of response proteins. Antitoxin and heat-shock proteins were activated for the global regulation of transcription and metabolism. Trigger factor Tig was upregulated to ensure proper initiation of transcription and aerobic respiration. Temperature-sensor protein VicR from the two-component system was used by the cell to regulate the composition of the cell wall and cell membrane. The over-consumption of metabolites, such as phosphoribosyl diphosphate (PRPP), purine nucleoside triphosphate (GTP), and acetyl-CoA forced the cells to assimilate more sugar for glycolysis. To this end, methyl-accepting chemotaxis proteins (MCPs) and sugar transportation protein PtsG were upregulated, simultaneously. Ultimately, peroxidase was activated to eliminate the redundant ROS, to minimize cell damage. These findings presented a system-level understanding of adaption processes of bacteria to antibiotic stress.