IJCRR - 3(11), November, 2011
Pages: 53-59
Print Article
Download XML Download PDF
LIPID PEROXIDATION IN PREGNANCY INDUCED HYPERTENSION
Author: Padmasree Dantu
Category: Healthcare
Abstract:Pre-eclampsia is due to reduced placental perfusion and a consequent maternal disorder
characterized by endothelial dysfunction caused by lipid peroxidation due to oxidative stress
secondary to reduced placental perfusion. An oxidative stress is said to occur when the
peroxidant injury due to lipid peroxides such as Malondialdehyde and secondary degeneration
products of lipid peroxidation overwhelms the antioxidant defence. The study was undertaken
to find out the levels of Serum Malondialdehyde in Pregnancy induced Hypertension (PIH).
A study was carried out among a total of 60 cases of PIH, distributed among the gestational
periods of 27-40 weeks. Controls were 75 normal pregnants and 30 non-pregnants. Serum
Malondialdehyde (MDA), Serum Total Cholesterol (TC), Serum Triglycerides (TG), Serum
High-density Lipoprotein Cholesterol (HDLC), Serum Low-density Lipoprotein Cholesterol
(LDLC), Serum Very Low-density Lipoprotein Cholesterol (VLDLC) were estimated. Other
investigations done were Urine Protein, Serum Creatinine, Serum Uric acid, Serum Glutamate
Oxaloacetate Transaminase (SGOT), Serum Glutamate Pyruvate Transaminase (SGPT) and
Serum Bilirubin in support of diagnosis. Malondialdehyde showed a definite increase with
increasing period of gestation in normal pregnant controls along with Serum Total Cholesterol,
Serum Triglycerides, and Serum Very Low-density Lipoprotein Cholesterol. In non-pregnant
controls, Malondialdehyde, Lipids and Lipid sub fractions were within the normal range. Serum
Malondialdehyde did not show any definite variation in relation to severity of disease like mild
without proteinuria, mild with proteinuria and severe PIH, but showed a definite increase with
increasing period of gestation 27-30 weeks, 31-35 weeks and 36-40 weeks. Serum Total
Cholesterol, Serum Triglycerides, Serum Very Low-density Lipoprotein cholesterol showed a
definite increase with increasing period of gestation in Pregnancy induced Hypertension.
Keywords: Endothelial dysfunction, Malondialdehyde, Oxidative stress.
Full Text:
INTRODUCTION
The major pathogenic mechanism in PIH is endothelial dysfunction related to reduced placental perfusion. Figure 1 Imbalance between vasodilator and vasoconstrictor endothelial factors as well as between thrombotic, fibrinolytic mediators and growth promoting substances leads to endothelial dysfunction. The major mechanism that promotes release of vasodilatory factors such as Nitric Oxide (NO), Prostacyclin (PGI2) and Endothelium Derived Hyper polarising Factor (EDHF) is the sheer stress blood flow on the endothelial surface.[1] Endothelial vasoconstrictors are Endothelin-1 and others like arachidonic acid products generated with cyclooxygenase participation: Prostaglandin F2, Thromboxane A2, Superoxide anion and Angiotensin II.[2] Oxidative stress is the term used to describe any challenge in which pro-oxidants predominate over antioxidants.[3,4] Oxidative damage of polyunsaturated fatty acids is lipid peroxidation [5,6], which causes a reduction in membrane fluidity, permeability and lowered NO synthesis leading to hypertension.[7] Lipid peroxidation has been implicated in the pathological process of PIH.[8,9] It is a chain reaction providing a continuous supply of free radicals that initiate further peroxidation. The primary molecular products of lipid peroxidation are unstable and aldehydes that are secondary stable products like Malondialdehyde (MDA) are produced which act as cytotoxic messengers. Lipid peroxidation of placenta has been studied as a model for phenomenon of aging. In PIH, there is increased lipid peroxidation in the maternal circulation and in the placenta (mitochondrial lipid peroxidation). MDA was assessed as a marker of lipid peroxidation and an index of degree of polyunsaturated fatty acid peroxidation. Increased placental VLDLC and LDLC could participate in endothelial dysfunction in PIH. A placental oxidant-antioxidant imbalance might cause the release of lipid peroxidation products into the circulation with subsequent damage of endothelium and increase of circulating lipid peroxide, which by themselves are able to induce smooth muscle constriction and increased pressor responsiveness to Angiotensin II. The increased susceptibility to oxidative stress of syncitiotrophoblast plasma membranes might be due either to reduced antioxidant system or to an abnormality of the lipid composition of the membranes.[10] Thus Serum MDA assay is useful to monitor the course of the disease.
References:
1. Born, M and Smith, T et al., Clinicians manual on endothelium and cardiovascular disease. London Science press, 1996.
2. Gavras, H and Gavras, L., endothelial function in cardiovascular disease. The role of Bradykinin. London Science. Press, 1996.
3. Jones, D.P. and Delong, M.J. Detoxification and protective functions of nutrients. Biochemical and physiological aspects of human nutrition. Ed. Stipanuk, MHWB Saunders Company, Philadelphia. P. 901-916, 2000.
4. Sies, H. Oxidative stress: Introductory remarks. Oxidative stress. Ed. Sies, H. Orlando, Florida: Academic press, p. 1- 10, 1985.
5. Ashok Mulchandani et al., Anal Biochem. 225,277-282, 1995.
6. Eum. J. B Boyle, J.A and Hearnsberger, J.O. J. Food Sci 59, 251- 255, 1994.
7. Mutlu, T urkoglu, U. et al., Plasma nitric oxide metabolites and lipid peroxide levels in preeclamptic pregnant women before and after delivery. Gynecol. Obstet. Invest, 48(4), 247-50, 1999.
8. Hallwell, B. and Gutteridge, J.M.C. Free radicals in Biology and Medicine 2ndEd Clarendon/oxford Univ. Press Oxford/Newyork, 416-494, 1989.
9. Halliwell B., Haemostasis 1, 118-126, 1993.
10. Cester, N. et al., Pregnancy induced hypertension: a role of peroxidation in microvillus plasma membranes. Mol. Cell. Biochem, 23, 131 (2), 151-5, Feb 1994.
11. Keisatoh., Serum lipid peroxide in cerebro vascular disorders determined by a new colorimetric method. Clin Chim. Acta, 90, 37-43, 1978.
12. Minoru Ishihara, et al., Studies on lipid peroxide of normal pregnant women and of patients with toxemia of pregnancy. Clin. Chim. Acta, 84, 1-9, 1978.
13. Mohanty, et al., VIII Annual National Conference, Ambicon, 1999.
|