Lipid peroxidation and antioxidant enzymes in male infertility.

BACKGROUND AND AIM: Mammalian spermatozoa are rich in polyunsaturated fatty acids and are very susceptible to attack by reactive oxygen species (ROS) and membrane lipid peroxide ion. Normally a balance is maintained between the amount of ROS produced and that scavenged. Cellular damage arises when this equilibrium is disturbed. A shift in the levels of ROS towards pro-oxidants in semen and vaginal secretions can induce an oxidative stress on spermatozoa. The aim was to study lipid peroxidation and antioxidant enzymes such as catalase, glutathione peroxidase and superoxide dismutase (SOD) and to correlate the same, with the 'water test', in male infertility. SETTINGS: Experimental study. SUBJECTS AND METHODS: Ejaculates from a total of 83 infertile and fertile healthy individuals were obtained. Lipid peroxidation and antioxidant enzyme levels were studied and correlated with water test. RESULTS: The results indicate that (i) the antioxidant enzyme catalase showed no significant changes in the various pathological samples, (ii) antioxidant enzymes SOD and glutathione peroxidase correlate positively with asthenozoospermic samples and (iii) the degree of lipid peroxidation also correlates positively with the poorly swollen sperm tails. The increase in SOD and glutathione peroxidase values, in the pathological cases represents an attempt made to overcome the reactive oxygen species. CONCLUSION: Water test could be used as a preliminary marker test for sperm tail damage by reactive oxygen species, since it correlates very well with lipid peroxidation and antioxidant enzymes.

Role of antioxidant defence in renal pathophysiology: primacy of glutathione peroxidase.

Antioxidant defences consisting of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and non-protein thiol (GSH) were estimated in the surviving kidney of unilaterally nephrectomized rats on days 1, 2, 3 and 12, following surgery. Simultaneously renal tissue lipid peroxidation (LP) and plasma GPx was monitored. The aim of this study was to evaluate the role of antioxidant defence in renal pathophysiology. Significant elevations in renal LP, GPx and GSH were evident on the first day and were maintained till 3rd day following nephrectomy. The response of SOD and catalase was slower, attaining significant elevation on 2nd and 3rd day respectively. Tissue GPx was the only parameter which remained elevated till 12th day, while all the other parameters returned to control levels by day 12. Plasma GPx declined significantly on days 3 (13.2%) and 12 (19.6%). These changes appear to be a part of the process when functions of 2 kidneys are taken over by a single kidney following unilateral nephrectomy.

Role of antioxidant enzyme defence in sparing rat hepatocytes from toxicity of ricin at low dose.

Ricin, a glycoprotein from castor oil seeds, is specifically toxic to Kupffer cells and at low doses it leaves parenchymal cells comparatively unaffected. At a dose of approximately 1.5 microgram/100 g body weight, ricin significantly increases the hepatic antioxidant enzyme system in rats within 24 hr. Superoxide dismutase, catalase and glutathione peroxidase show an increase in liver tissue levels of 19-24%. However, hepatic lipid peroxidation is elevated by about 34% and non-protein sulphydryl is reduced by 26%. The enhanced levels of antioxidant enzymes appear to protect the hepatocytes from the toxin. The observed elevation of hepatic thiobarbituric acid-reactive substances appears to originate mainly from the damaged Kupffer cells.

Effect of ricin on acute phase response in rats.

Ricin, a highly toxic protein from castor beans was administered (ip) to rats in a dose of 1.25 micrograms/100 g to selectively deplete at least 60-70% of Kupffer cells. This dose spared hepatocytes. This rat model was used to study acute phase protein synthesis and the role of Kupffer cells in acute phase response (APR). Ricin itself induced an APR, similar in pattern but of lower magnitude, than that induced by turpentine. However, the effect of combination of ricin and turpentine on APR was not additive. Kupffer cells appear to play permissive role in APR through mediators like hepatocytes stimulating factors.

Biokinetics of 99mTc-labelled liver-imaging agents in an animal model of liver cirrhosis.

Comparable degree of liver cirrhosis, as judged by liver function tests and histopathology, was induced in rats by carbon tetrachloride. Comparative organ distribution of 99mTc-sulphur colloid and 99mTc-phytate was studied in the liver, spleen and lungs of these cirrhotic rats. Compared to controls, the biodistribution of 99mTc-sulphur colloid was found to be affected more than that of 99mTc-phytate in cirrhotic rats, especially at early time intervals.

Plasma orosomucoid metabolism and susceptibility to malarial infection in rodents.

The effects of Plasmodium berghei infection on liver function and plasma orosomucoid metabolism were investigated in Wistar rats. Infected rats with 20-25% parasitaemia manifested increased serum transaminase levels, hypoalbuminaemia and hypoproteinaemia. In spite of such indications of deranged liver function, the hepatic synthesis rate (as measured by 14C-amino acid incorporation) of seromucoids predominantly orosomucoid or alpha 1-acid glycoprotein) was increased by 73%. The circulating levels of this glycoprotein were also doubled in infected animals. The albumin synthesis rate was not increased. This preferential synthesis and increase in circulating levels of orosomucoid may have in vivo significance in malarial infection, in view of reports that orosomuocid has influence on in vitro invasion of red cells by malarial parasites.

Quantitation of gastrointestinal protein loss.

Plasma proteins leak into the gastrointestinal tract under physiological conditions. This may assume enormous proportions in certain pathological conditions associated with the stomach, intestines, intestinal lymphatics and capillaries, resulting in severe hypoproteinemia. Quantitation of this leakage has been achieved by using plasma proteins or non-protein foreign colloids and macromolecules labelled with radioactive isotopes. The requirements of an ideal label have been listed and the advantages/disadvantages of different tracer labels have been reviewed. No label presently available fulfils all the requirements of an ideal tracer. In spite of this, a wealth of information has been acquired by gastroenterologists to unravel the mystery of hypoproteinemia of unknown cause.

Liver function and plasma protein metabolism in rodent model of filariasis.

Rodent model of filariasis was developed by infecting Wistar rats with Litomosoides carinii. Liver function tests, plasma protein concentrations, and synthesis rates of liver-formed proteins were estimated in these rats at 63 and 90 days post-infection. At 63 days post-infection, aspartate aminotransferase and alkaline phosphatase were significantly increased. Alanine aminotransferase, plasma total proteins and plasma albumin were in the normal range. However, at 90 days post-infection all these parameters were affected, reflecting progressive liver involvement. Hypoalbuminemia at 90 days post-infection did not appear to be due to decreased synthesis rate, indicating higher catabolism and/or altered distribution in pools.