Analysis of the chemical components from the culture broth of the marine bacterium Saccharomonospora sp. CNQ-490 has yielded three novel compounds: saccharobisindole (1), neoasterric methyl ester (2), and 7-chloro-4(1H)-quinolone (3), in addition to acremonidine E (4), pinselin (5), penicitrinon A (6), and penicitrinon E (7). The chemical structures of the three novel compounds were elucidated by the interpretation of 1D, 2D nuclear magnetic resonance (NMR), and high-resolution mass spectrometry (HRMS) data. Compound 2 generated weak inhibition activity against Bacillus subtilis KCTC2441 and Staphylococcus aureus KCTC1927 at concentrations of 32 μg/mL and 64 μg/mL, respectively, whereas compounds 1 and 3 did not have any observable effects. In addition, compound 2 displayed weak anti-quorum sensing (QS) effects against S. aureus KCTC1927 and Micrococcus luteus SCO560.

An ubiquinone derivative, pseudoalteromone A (1), has been isolated from two marine-derived Pseudoalteromonas spp., APmarine002 and ROA-050, and its anti-melanogenesis activity was investigated. The anti-melanogenic capacity of pseudoalteromone A was demonstrated by assessing the intracellular and extracellular melanin content and cellular tyrosinase activity in the B16 cell line, Melan-a mouse melanocyte cell line, and MNT-1 human malignant melanoma cell line. Treatment with pseudoalteromone A (40 μg/mL) for 72 h reduced α-melanocyte-stimulating hormone (α-MSH)-induced intracellular melanin production by up to 44.68% in B16 cells and 38.24% in MNT-1 cells. Notably, pseudoalteromone A induced a concentration-dependent reduction in cellular tyrosinase activity in B16 cell, and Western blot analyses showed that this inhibitory activity was associated with a significant decrease in protein levels of tyrosinase and tyrosinase-related protein 1 (Tyrp-1), suggesting that pseudoalteromone A exerts its anti-melanogenesis activity through effects on melanogenic genes. We further evaluated the skin-whitening effect of pseudoalteromone A in the three-dimensional (3D) pigmented-epidermis model, MelanoDerm, and visualized the 3D distribution of melanin by two-photon excited fluorescence imaging in this human skin equivalent. Collectively, our findings suggest that pseudoalteromone A inhibits tyrosinase activity and expression and that this accounts for its anti-melanogenic effects in melanocytes.

An ethyl acetate extract from the deep-sea bacterium Galbibacter orientalis strain ROD011 (GOEE), collected from international waters, was investigated as a potential anti-inflammatory agent. In lipopolysaccharide (LPS)-stimulated murine macrophages, nitric oxide (NO) production fell by 72–87% at 5–20 µg/mL GOEE without detectable cytotoxicity. Cyclooxygenase-2 (COX-2 protein abundance decreased in a dose-dependent manner and was nearly absent at 20 µg/mL. In zebrafish embryos, survival was maintained up to 40 µg/mL, and LPS-induced signals were attenuated; the cell-death rate declined from 10 µg/mL onward, and at 20 µg/mL GOEE, reactive oxygen species (ROS) and NO decreased by 85% and 27%, respectively. To explain these effects, untargeted metabolomics with pathway enrichment and network mapping were performed in LPS-driven macrophages. Of the 58 KEGG pathways evaluated, 18 reached significance, notably purine and pyrimidine metabolism, vitamin B6 metabolism, and the one-carbon pool via folate. Coordinated shifts also involved amino-acid/tricarboxylic acid (TCA)-cycle linkages, glutathione and glyoxylate/dicarboxylate, and sphingolipid pathways. Network analysis identified hubs that were concomitantly reprogrammed. Collectively, GOEE achieved multi-level suppression of inflammatory outputs while preserving viability, and the metabolomic signature provides a mechanistic scaffold for its action. These findings nominate a deep-sea microbial extract as a promising anti-inflammatory lead and motivate fractionation and targeted validation of the highlighted metabolic nodes.