In this work, we have investigated the washing performance of sodium oxalate-based detergents containing different enzymes (protease, lipase and cellulase). The results show that sodium oxalate-based detergents with enzymes have a better washing performance than formulations containing the conventional builder STPP and zeolite 4A. For sodium oxalate-based with protease, the amount of sodium oxalate and protease have a significant effect on the detergency. Lipase can improve detergency of sodium oxalate-based detergents after “first washing” in the presence of different anionic surfactant (LAS, MES and AES). For cellulase, only sodium oxalate in the presence of LAS has a detergency increase.
The builder is an important ingredient in detergents. Sodium oxalate is a good non-phosphate detergent builder, which has good calcium-removing properties and good wash performance in detergents. However, sodium oxalate-based detergent formulations face a tricky problem of “incrustation” on fabrics due to calcium oxalate deposition. If sodium oxalate is used in commercial detergents, then “incrustation” must be solved. In this study, we examined the effect of fabric type, anionic surfactant, polymer, and temperature on incrustation and soil redeposition (“secondary” washing effect) of a sodium oxalate-based detergent. The results showed that both the anionic surfactant and polymer influenced the deposition of calcium oxalate on fabrics. Overall, the amount of calcium oxalate deposition followed the order polyamide < polyester < cotton with the same formulation. Finally, good secondary washing effects (low ash deposition and high whiteness retention) formulations were selected by cumulative washing. The formulation of methyl ester sulfonate (MES)-sodium carboxymethyl cellulose (CMC), MES-polyvinyl pyrrolidone, and alcohol ether sulfate (AES)-CMC had better secondary effects, and the optimal combination of the 12 formulations was AES-CMC.
Jingyi Li,Ziyu Chen,Mingming Jin,Xuefeng Gu,Yuhan Wang,Gang Huang,Weiming Zhao,Changlian Lu
Lactylation, a newly identified post-translational modification, is uncertain in its implication in triple-negative breast cancer (TNBC). In this study, we analyzed 60 TNBC samples using immunohistochemical staining and revealed elevated levels of pan-lactylated proteins and specific histone H4K12 lactylation in tumor tissues, correlating with TNBC progression. Lactate exposure in TNBC cell lines significantly induced lysine lactylation at the H4K12 site, leading to alterations in gene profiles and reduced apoptosis. These effects were attenuated by DCA or sodium Oxamate, inhibitors of endogenous lactate production. Gene sequencing showed an increase in Schlafen 5 (SLFN5) expression in TNBC cells treated with Oxamate, contrasting with the effects of lactate exposure. Analysis of TNBC tissues showed a negative correlation between H4K12 lactylation and SLFN5 protein levels. Overexpression of SLFN5 countered the effects of lactate on apoptosis and tumor growth, highlighting its pivotal role in TNBC malignancy. CUT&Tag sequencing indicated that lactylated H4K12 potentially binds to the SLFN5 promoter region. Luciferase reporter assays further verified that lactate-induced suppression of SLFN5 promoter activity is mediated by wild-type H4K12, but not by its R or A mutants, verified by both in vitro and in vivo apoptosis detection in response to lactate and Oxamate stimulation. These results establish that H4K12 lactylation, induced by lactate in TNBC cells, specifically suppresses SLFN5 expression, contributing to TNBC malignancy. Our findings illuminate a critical histone lactylation-dependent carcinogenic pathway in TNBC.
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