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Year : 2002  |  Volume : 50  |  Issue : 3  |  Page : 375-6

Value of sialic acid level in newborn infants with perinatal asphyxia.






How to cite this article:
Ycaoasyoolu D, Caksen H, Yyldyz B, Cetinkaya O. Value of sialic acid level in newborn infants with perinatal asphyxia. Neurol India 2002;50:375


How to cite this URL:
Ycaoasyoolu D, Caksen H, Yyldyz B, Cetinkaya O. Value of sialic acid level in newborn infants with perinatal asphyxia. Neurol India [serial online] 2002 [cited 2023 Feb 3];50:375. Available from: https://www.neurologyindia.com/text.asp?2002/50/3/375/1416



Gangliosides are carbohydrate-rich complex lipids of large size and great complexity which are found in cell membranes, especially neuronal cell membranes. The hydrophobic moiety, consisting of sphingosine and fatty acid (stearic acid, 95%), is inserted into the membrane, while the hydrophilic moiety, consisting of sialic acid [N-asetile noraminic acid (NANA)] and other carbohydrates, protrudes towards the extracellular fluid.[1] Although the molecular mechanism(s) and the substrates for the neurotrophic activity of the gangliosides are not fully understood, the published experimental work suggests that monosialoganglioside (GM1) has antineurotoxic, neuroprotective, and neurorestorative effects on various central neurotransmitter systems.[2] In this article, we studied serum total sialic acid (TSA) levels in newborn infants with perinatal asphyxia to determine whether there was a relationship between perinatal asphyxia and TSA. To our knowledge this is the first study in the literature.
The study includes 44 newborn infants with perinatal asphyxia and 31 healthy infants selected as control group. Serum TSA levels were studied 24 hours after the birth in the infants because neuronal death develops at that time. Serum TSA levels were studied by spectrophotometric method.[3] There was no statistically significant difference between the groups for gestational age, gender and birth weight (p >0.05) [Table - 1]. However, serum TSA level was 101.639.78 mg/dl and 108.1612.64 mg/dl in the control and study group respectively (p <0.05). There was a statistically significant difference for serum TSA levels between the groups. We also investigated the relationship between the clinical severity of perinatal asphyxia and serum TSA levels. Of 44 infants with perinatal asphyxia, 18 infants were in stage 1 (mild), 15 infants in stage 2 (moderate) and 11 infants in stage 3 (severe). Serum TSA levels were 103.756.86 mg/dl, 111.1317.92 mg/dl and 111.319.90 mg/dl, respectively. There was a statistically significant difference among the subgroups (p <0.05). Serum TSA levels in infants in stage 1 were the lowest, and similar to those of control group (p >0.05). However, serum TSA levels in infants in stage 2 and 3 were higher than those of control group and a significantly difference was found (p <0.05).
Although gangliosides were discovered some 50 years ago, their potential role in neuronal functions has been appreciated only recently. During development, their composition and concentration change in both a variety of animal species and humans.[1] Their role is indicated from studies which have shown that abnormalities in ganglioside metabolism can have a severe impairing effect on normal development.[1]
Although it was noted that GM1 can protect the fetal brain against hypoxic-ischemic injury in animal studies,[4] Katoh-Semba et al[5] showed, on rat cerebrum, that ganglioside was not itself responsible for the restricted astroglial cell proliferative response, as serum produced the same behaviors. Even though our findings showed that serum TSA, levels were elevated in infants with perinatal asphyxia and infants with clinically severe perinatal asphyxia had significantly higher levels of TSA than those of infants with moderate and mild perinatal asphyxia, further studies are needed to verify these results.


 

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1.Gorio A : Ganglioside enhancement of neuronal differentiation, plasticity, and repair. Crit Rev Clin Neurobiol 1986; 2: 241-296.   Back to cited text no. 1    
2.Hadjiconstantinou M, Neff NH : GM1 ganglioside: in vivo and in vitro trophic actions on central neurotransmitter systems. J Neurochem 1998; 70: 1335-1345.   Back to cited text no. 2    
3.Barry GT, Abbott V, Tsai T : Relationship of colonimic acid (poly N-acetylneurominic acid) to bacteria which contain neurominic acid. J Gen Microbiol 1962; 29: 335-352.   Back to cited text no. 3    
4.Tan WK, Williams CE, Gunn AJ et al : Pretreatment with monosialoganglioside GM1 protects the brain of fetal sheep against hypoxic-ischemic injury without causing systemic compromise. Pediatr Res 1993; 34: 18-22.   Back to cited text no. 4    
5.Katoh-Semba R, Facci L, Skaper SD et al : Gangliosides stimulate astroglial cell proliferation in the absence of serum. J Cell Physiol 1986; 126: 147-153.   Back to cited text no. 5    

 

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