Bladder microsomal enzymes in health and disease

The bioactivation of N-nitrosamines and polycyclic aromatic hydrocarbons [PAHs] is mediated primarily by the mixed-function oxidase system, which includes dimethylnitrosamine N-demethylase I, arylhydrocarbon hydroxylase, cytochrome P-450, cytochrome b[5], and ethoxycoumarin deethylase. Most of carcinogens and xenobiotics are conjugated and detoxified by phase II drug-metabolizing enzymes such as glutathione S-transferase. The present study showed the influence of Schistosoma haematobium on the activity of the above-mentioned enzymes in thirteen schistosome-infected human bladder tissues compared with those of fifteen schistosome-free samples. The contents of cytochrome P-450 and cytochrome b[5] increased in the bladder 157 tissues by 48% and 69% respectively. Moreover, the activities of dimethylnitrosamine N-demethylase I and arylhydrocarbon hydroxylase, ethoxycoumarin O-deethylase, ethoxyresorufin O-deethylase, and pentoxyresorufin O-depentylase increased by 75%, 159%, 49%, 63% and 44% respectively. The signal intensity for cytochrome P-450 2E1 was greatly increased over the control. The present study clearly demonstrated that S. haematobium changes the activity of carcinogen-metabolizing enzymes. We conclude that S. haematobium could enhance the carcinogenicity of polycyclic aromatic hydrocarbons [e.g. benzo[a]pyrene] and N-nitrosamines in the human bladder tissues, and probably other tissues, since there is an association between schistosomiasis and bladder cancer

Lipid peroxidation and glutathione redox system in human bladder tissues infected with schistosoma haematobium

The present study was carried on human bladder tissues infected with schistosoma haematobium to demonstrate the effects of schistosomiasis on lipid peroxidation and gluathione redox system. Bladder tissue samples were collected from 15 individuals free of schistosomiasis infection and 13 individuals infected with schistosomiasis. Schistosomal bladder specimens were histologically verified by the presence of schistosomal haematobium ova and schistosomal cystitis in bladder mucosa. The biochemical analysis of infected bladder tissues revealed that thio-barbituric acid reactant substances [TBARS], an intermediate product of the oxidation of polyunsaturated fatty acids, increase significantly by + 125% [P < 0.001]. On the other hand, the levels of reduced glutathione [GSH] and the activity of glutatione reductase decreased significantly by 57% [P < 0.01] and - 40% [P<0.001] respectively. Also, the activity of glutathione S - transferase [GST] increased significantly by + 89% [P<0.001]. In conclusion, these results indicate that schistosoma haematobium infection of human bladder tissues induce marked lipid peroxidation damage due to disruption of glurathione redox system

Polyacrylamide gel electrophoretic pattern of urinary and serum proteins in some chronic renal diseases

In this study, urinary and serum proteins in control, CRF and nephrotic groups are fractionated into 11 fractions arranged from the anodal side on polyacrylamide gel electrophoressis. Statistical analysis of the results revealed that: 1- In chronic renal failure group, both quantitative and qualitative changes in serum and urinary proteins occur. There is a very highly significant increase in urinary total proteins, F1[1] F[5] and F[6] as well as a highly significant increase in urinary F4 and a significant increase in urinary F[2]. On the other hand there is a highly significant decrease in serum total proteins and F6. Also, there is a highly significant decrease in F[2] and F[6]. On the other hand, there is a highIy significant increase in serum F1 and F9. F10 and F11 are present only in CRF group but not in control or nephrotic groups. 2- In nephrotic group, there is a very highly significant increase in urinary total proteins, F1, F3, F5 and F6 as well as a highly significant increase in F[2]. The urinary protein F7, F8 and F9 are present in nephrotic group but F[10] and F[11] are absent. As for serum, there is a very highly significant decrease in serum total proteins. F[2] and F[6]. a highly significant decrease in F[5] and a significant increase in F9 and absence of F[10] and F11 which are present in CRF group only. 3 In CRF group, there is a highly significant increase in serum F 1, which may be B2 microglobulin and may be of value in the genesis of symptoms in CRF. 4 Considering urinary F3, which is most probably transferrin, it showed a very highly significant increase in nephrotic group, but insignificant change in CRF group. So, it may be considered as an indicator for pathological glomerular proteinuria. 5 As regards urinary F4 which is most probably B-globulin, it showed a highly significant increase in CRF group but insignificant change in nephrotic group. This may be of value in diagnosis and differntiation between CRF and nephrotic syndrome.6- F7, F8 and F9 are most probably IgM. These fractions are present in urine of CRF and nephrotic group, but absent in urine of control group because they can not pass through the normal glomerular membrane. 7- There is a highly significant increase in serum F9 in CRF group. This fraction is of a large molecular weight and essentially unfilterable and may have a role in the genesis of renal failure symptoms. It is concluded that fraction of urinary as well as serum proteins by polyacrylamide gel electrophoresis may be of high value in diagnosis and prognosis of renal disease status. The increase in urinary F3 is an indicator of glomerular proteinuria which occurs in nephrotic syndrome and the increase in urinary F4 is an indicator of tubular proteinuria and may be of diagnostic value in chronic renal failure