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Macronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Sphingolipids constitute a class of lipids defined by their 18 carbon-amino-alcohol backbones which are synthesized in the endoplasmic reticulum from non-sphingolipid precursors (66, 117). In sphingolipids, glycerol is replaced by a group of aliphatic amino alcohol named sphingosine that contains two alcohols with the middle position occupied by an amine. Sphingolipids are complex lipids which yield fatty acids, sphingosine, phosphoric acid, and an alcohol component upon hydrolysis. A sphingosine has three parts, a three carbon chain with two alcohols and amine attached and a long hydrocarbon chain containing 12–22 carbon atoms (69, 115, 117). The main and abundant component of sphingolipids in animals is sphingomyelin that constitutes the membranous myelin sheath surrounding nerve cell axons (114, 117). Sphingomyelin usually consists of a sphingosine linked to a long chain fatty acyl chain called ceramide and attached to a phosphocholine group at the primary alcohol group of a sphingosine (66, 117). Precisely, ceramide is amide of fatty acids with sphingosine. So, sphingomyelin can also be classified as sphingophospholipid (115). Like glycerophospholipids and cholesterol, sphingolipids are ubiquitous in the body and found in every cell membrane, particularly nerve cells and brain tissues (114–117).
Lysosomal Ion Channels and Human Diseases
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Peng Huang, Mengnan Xu, Yi Wu, Xian-Ping Dong
Pharmacologically, in addition to TPC2-A1-N, TPC2-A1-P, LyNa-VA and LyNA, all three TPCs are insensitive to the voltage-gated Na+ channel blocker tetrodotoxin (TTX) but sensitive to voltage-gated Ca2+ channel blockers including verapamil, Cd2+, and nifedipine (Cang et al., 2013, 2014a,b; Wang et al., 2012). Sphingosines were also reported to induce TPC1-mediated Ca2+ release from the lysosome (Hoglinger et al., 2015). However, electrophysiological assay suggests that sphingosine may activate TPCs indirectly (Li et al., 2019; Zhang et al., 2019).
Atopic Dermatitis
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Luz Fonacier, Amanda Schneider
Atopic dermatitis has a pathogenesis of complex immune dysregulation and interplay of genetic, environmental, epidermal and psychological factors. The stratum corneum of healthy skin functions as a barrier and provides water-retaining properties. It contains an extracellular lipid matrix including ceramides, cholesterol and free fatty acids (Leung 2001). When this layer becomes dry and fissured, it becomes a portal of entry for bacteria, mostly commonly Staphylococcus aureus. Disruption of the integrity of the stratum corneum exposes epidermal and dermal extracellular matrix proteins, such as fibronectin and collagen which can serve as anchors for S. aureus binding via adhesions (Cho et al. 2001). In AD, the stratum corneum lipid composition contains decreased levels of ceramides and sphingosine which normally act as water-retaining molecules. Deficient ceramide increases secretion of ceramidases, which leads to increased transepidermal water loss, resulting in dry, cracked skin of AD (Cardona et al. 2006, Arikawa et al. 2002). Sphingosine has been shown to normally possess antimicrobial properties, thus deficiencies may favor bacterial colonization (Arikawa et al. 2002).
Effect of sphingosine and inoculum concentrations on Staphylococcus aureus and Staphylococcus epidermidis biofilms
Published in Biofouling, 2023
Minyoung Kim, Jada S. McMahon, Julianna M. Nerone, Luciana H. Skinner, Guy K. German, Cláudia N. H. Marques
As with any physiological system, the interactions between the ceramides, cutaneous immunity, keratinocytes, corneocytes, and the microbiome involved in AD are intricate (Kim and Kim 2019; Blicharz et al. 2021; Lefèvre-Utile et al. 2021). Such complexity is further confounded by the interactions between each species present within the microbiome. In this study, the relationship between S. aureus and S. epidermidis viability, and sphingosine was determined. To achieve this, the only different variables were the population ratio between S. aureus and S. epidermidis, and the change of sphingosine concentration. The varying levels of sphingosine used in this work were based on the concentrations previously reported to occur in healthy skin and AD-affected skin: the condition in which sphingosine was at a concentration of 80 mg/L was labeled ‘normal sphingosine’, whereas 45 mg/L was labeled ‘AD sphingosine’ (Arikawa et al. 2002). Likewise, the conditions of the microbiome on healthy and AD-affected skin were reflected in the relative concentrations of S. epidermidis and S. aureus, where the ratio in which S. epidermidis was the dominant organism was labeled ‘normal ratio’, and the inverse was labeled ‘AD ratio’ (Kong et al. 2012; Allen et al. 2014; Salava and Lauerma 2014; Williams and Gallo 2015; Byrd et al. 2017; Blicharz et al. 2021).
Assessing potential liver injury induced by Polygonum multiflorum using potential biomarkers via targeted sphingolipidomics
Published in Pharmaceutical Biology, 2022
Zhixin Jia, Lirong Liu, Jie Liu, Cong Fang, Mingxia Pan, Jingxuan Zhang, Yueting Li, Zhong Xian, Hongbin Xiao
Sphingolipid (SPL) play an important role in cell survival and death (Cuvillier et al. 1996) as well as the progression of liver diseases and hepatic dysfunction. Figure 1 shows the metabolic pathway of SPLs (Merrill et al. 2009; Lebesgue et al. 2017). Sphingosine could cause cell apoptosis and senescence, whereas sphingosine-1-phosphate (S1P) and ceramide-1-phosphate (C1P) promote cell growth and proliferation (Gómez-Muñoz 2006; Rodriguez-Cuenca et al. 2017). Moreover, the perturbations of plasma SPLs could be related to hepatocyte apoptosis and liver injury (Neumeyer et al. 2006). Apoptosis mediated by the mitochondria in liver cells could cause the accumulation of plasma ceramides (Cers) and a decrease in dihydroceramides (dhCers) (Stiban et al. 2006; Park et al. 2013; Pastore et al. 2015). Therefore, SPLs detection might be an applicable approach to detecting PM-induced liver injury.
Mycotoxin exposure and pregnancy
Published in Critical Reviews in Toxicology, 2020
İlknur Münevver Gönenç, Neslihan Yilmaz Sezer, Serkan Yilmaz
Due to ability to cross the placenta, mycotoxins can have a negative effect on the fetus and lead to malformation of the central nervous system and harmful to the brain (Omotayo et al. 2019). Using proxy measures for the exposure of mycotoxins, one study in Norway investigated hypospadias and cryptorchidism, which are urogenital birth defects in males, as outcomes. Children of grain farmers, who were exposed to two or more fungal metabolites during conception season, were determined to have these defects more commonly (PR hypospadias 1.80; 95% CI 0.90–3.40; PR-cryptorchidism 1.2; 95% CI 0.60–2.40) when compared to those who were exposed to just one or no mycotoxin at all. Yet, the findings were consistent and there was no difference between the groups (Kristensen et al. 2000). To identify if maternal fumonisin exposure was associated with NTDs in neonates during pregnancy, Missmer et al. (2006) carried out a population-based case–control study among Mexican-American women who delivered neonates with NTDs from 1995 to 2000. The maternal blood FB levels were determined using the proportion of sphinganine/sphingosine (sa:so) in the blood. This rate was linked to the risk of neural tube defects (ORrange 1.5–4.5); for example, spina bifida, with a maximum sa:so ratio of 0.35. Fetal death was more likely beyond this value. Exposure to fumonisin, as suggested by the authors of the study, increases the risk of NTD to a threshold level, in proportion to the dose, beyond which fetal death may be more likely (Missmer et al. 2006).