Effect of ascorbic acid on hyaluronidase inhibitor.

Abstract

THE presence of a physiological inhibitor of hyaluronidase (PHI) in mammalian serum was suggested by Duran-Reynals1 who observed the destruction of spreading factor by blood. Hobby et al.2 and McClean3 later reported the inhibition of microbial and mammalian hyaluronidase by serum. PHI, which is a glycoprotein and sensitive to heat4, has been shown to increase in both bacterial and viral infections, cancer and various liver, kidney and rheumatic diseases4,5. A small increase of PHI has been reported in scorbutic guinea pigs by Shack et al.6. These increases have been suggested5,8 to represent a defence against invasive microorganisms, or a non-specific response to tissue inflammation or destruction4. (Fiszer-Szafarz7 described a hyaluronidase inhibitor in the serum of cancer patients which she believes is different from PHI.) Cameron and Pauling suggested that a high intake of ascorbic acid increases the biosynthesis of PHI, resulting in a decrease in hyaluronidase activity9. Consequently, the invasiveness of proliferative diseases would be prevented by reduced depolymerisation of the intercellular matrix of the proliferating cells. We have investigated the effect of doses of ascorbic acid of 0–1,000 mg kg−1 d−1 on levels of PHI in the serum of guinea pigs. Our results show that PHI is not affected by high levels of dietary ascorbic acid.