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Abstract

Contents of sphingenine (sphingosine) and sphinganine were studied in sphingomyelins of transplantable mouse tumors (hepatoma-22, melanoma B16, Lewis lung carcinoma, intestine carcinoma) and rat nephroma RA. The content of sphinganine was increased in sphingomyelins of hepatoma-22 and nephroma RA compared to sphingomyelins of liver and kidneys. Significant contents of sphinganine were also found in sphingomyelins of other studied tumors. The content of sphinganine in regenerating mouse liver (30 h after hepatectomy) was normal. The data suggest that disorders should exist in biosynthesis of sphingoid bases in tumors but not in normal rapidly proliferating tissue.

A Novel Lipidomic Strategy Reveals Plasma Phospholipid Signatures Associated with Respiratory Disease Severity in Cystic Fibrosis Patients

“…Sphinganine is the saturated form of sphingosine, both sphingoid base components of sphingomyelins. Sphinganine-containing molecules are elevated in malignant tumors as compared to normal tissues [40], and a higher content can be attributed to a decrease in dihydroceramide desaturase activity. However, no information is available on plasma levels of these compounds.…”

Sphingolipid abnormalities in cancer multidrug resistance: Chicken or egg?

“…In hepatoma, C16:1 SM was present in higher percentage compared with normal liver tissue [231] while all SM species tested were elevated in cancerous versus adjacent normal breast tissue, though C16:1 SM was not investigated [222]. Furthermore, SM species with a sphinganine base were increased in multiple tumors including hepatoma and nephroma compared with regenerating mouse liver [232]. In addition to deregulation of sphingolipid metabolism and SM accumulation in cancerous cells transforming from healthy, differentiated cells, SM-enriched tumor cells could also be derived from stem cells or rare precursors.…”

The Role of Sphingolipid Metabolism in Bone Remodeling

“…Ceramide is a bioactive lipid that serves as a second messenger in the regulation of cell death pathways and metabolism in response to stress, apoptotic triggers, and chemotherapy ( Ryland et al, 2011 ; Kurek et al, 2013 ), involving extrinsic mechanism by mimicking the cytotoxicity of TNF ( Hannun, 1994 ), and an intrinsic mechanism by modifying enzymes to regulate the level of ceramide ( Morales et al, 2007 ), further leading to signal cascade and cell death by the downstream of Bcl2. However, S1P opposes the proapoptotic function of ceramide ( Rutherford et al, 2013 ) and the ratio of S1P and ceramide is described as a rheostat of sphingolipid which is involved in the pathogenesis of certain cancers and this rheostat is one of the targets of anticancer drugs ( Dyatlovitskaya et al, 2001 ). Ceramide plays an important role in bone metabolism.…”