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S L Alade

Publications and source records attributed to S L Alade.

5 recordsLinked to original sources
PubMed1989

Lipoperoxidation and T-cell leukemia of childhood. Effects of indomethacin.

Serum thiobarbituric acid (TBA) reactivity for lipoperoxidation products was assessed at diagnosis in children with T-cell and common acute lymphocytic leukemia (ALL) and T-lymphoblastic lymphoma. Comparisons were made among these groups and with healthy controls. Mean TBA reactivity (mumol malondialdehyde/L serum) was increased (P less than 0.01) in the T-cell leukemia group versus common ALL and T-lymphoblastic lymphoma patients and controls, respectively. The increase in lipoperoxidation products in T-cell ALL appeared to bear a positive relation to peripheral leukocyte counts, and was accompanied by increased serum prostaglandin E2 (PGE2) levels in most representative cases. Indomethacin added to a childhood T-cell ALL line (SUP-T3), at a concentration known to inhibit prostaglandin synthesis in vitro (i.e., 3 micrograms/mL), effected significant increases in the numbers of natural killer (NK; Leu-11+ and Leu-19+) cells (P less than 0.01) and B-lymphocytes (P less than 0.05), and significant decreases in cell viability (P less than 0.01). Indomethacin may be a useful agent for enhancing the antileukemic immune response in T-cell ALL.

Child↗
PubMed1988

Serum lipoperoxidation products in an infant with hemolytic-uremic syndrome.

We detected increased concentrations of lipoperoxidation products, as malondialdehyde, in the serum of an infant with classic hemolytic-uremic syndrome. The concentrations declined when peritoneal dialysis was initiated and eventually returned to normal after clinical recovery. Our observation adds to the existing body of evidence that links the pathogenesis of hemolytic-uremic syndrome to peroxidative damage and to the rationale for using antioxidant agents as part of the therapy for this disease process.

Hemolytic-Uremic Syndrome↗
PubMed1986

Polysorbate 80 and E-Ferol toxicity.

The relatively recent introduction and use of an intravenous form of a vitamin E preparation (E-Ferol) has been associated with the development of an unusual syndrome and fatalities among low birth weight (less than 1,500 g), premature infants in neonatal intensive care units. We have observed an inhibitory effect by this vitamin E preparation on the in vitro response of human lymphocytes to phytohemagglutinin (PHA). E-Ferol suppressed the expected response to low doses of PHA. However, this suppression was not due to the alpha-tocopherol acetate (vitamin E) component, because alpha-tocopherol acetate by itself was not inhibitory; in fact, it often enhanced the PHA response. Because a mixture of polysorbate 80 and polysorbate 20 is used as a carrier in E-Ferol, these components were also tested and were found to be responsible for the suppression, especially the polysorbate 80. Concurrent with this suppression of PHA-induced mitogenesis was a decrease in the percentage of T11 lymphocytes.

Humans↗
PubMedDate not supplied

Serum vitamin A status in acute lymphocytic leukemia of childhood.

Serum vitamin A status was assessed at the diagnosis in 31 children with common acute lymphocytic leukemia (CALL) and seven with T-cell leukemia (T-ALL). A control population consisting of 22 children was established to serve as one basis for comparison. Mean concentrations of vitamin A, retinol-binding protein (RBP) and prealbumin (PA) were significantly less (p less than 0.01) in the sera of patients with T-ALL when compared with the controls. Similarly, mean RBP and PA levels were reduced (p less than 0.01) in the sera of patients with CALL. In addition, "euretinolemic" and "hyporetinolemic" subgroups of CALL were identified comprising 74.2 percent and 25.8 percent of the patient population, respectively. The latter differed from the euretinolemic patients by being younger and showing an even greater decrease in the serum concentrations of RBP and PA. These findings indicate that there are factors affecting carrier proteins of vitamin A in childhood T-cell and common ALL; also, the data provide further evidence of the heterogeneity of common acute lymphocytic leukemia of childhood.

Child↗