ABSTRACT
Status of oxidative/antioxidative profile was the mechanistic approach to inumerate the nature of protection by N-acetylcysteine (NAC) in isoniazid (INH) exposed experimental animals. Analysis of lipid peroxidation, thiol levels, cytochrome P450, superoxide dismutase (SOD), catalase, glutathione peroxidase, reductase and transferase were estimated in liver along with the body and liver weight of animals and histological observations. Isoniazid exposure to animals resulted in no change in body and liver weights. Thiols, lipid peroxidation, catalase, SOD glutathione peroxidase, reductase, transferase and cytochrome P450 levels were altered with INH exposure. Supplementation of NAC with INH protected the animals against hepatotoxic reactions by minimizing the free radical induced tissue injury and overall maintenance of the endogenous scavengers of free radicals.
Subject(s)
Acetylcysteine/pharmacology , Animals , Antioxidants/metabolism , Free Radical Scavengers/metabolism , Glutathione/metabolism , Isoniazid/antagonists & inhibitors , Liver/drug effects , Male , Oxidants/toxicity , Rats , Rats, WistarABSTRACT
The binding of 125I labelled IgG to the microvillus membranes (MVM) has been studied during postnatal development of rat intestine. The levels of mRNA encoding IgG receptor were also analyzed by liquid hybridization under these conditions. The IgG binding to MVM reached maximum levels by day 12 and showed a gradual decline upon weaning. The FcRn mRNA was markedly low in adult rats and was maximum during second week of postnatal development. Administration of cortisone or thyroxine to suckling rats, induced precocious decline of both IgG binding and the receptor expression. However, insulin administration did not affect the receptor expression. Scatchard analysis of IgG binding to MVM in cortisone injected pups revealed that the observed inhibition in IgG binding was a consequence of a decrease, both in the affinity constant (-Ka) as well as in the number of receptor sites (n) while thyroxine administration caused a reduction in the number of receptor sites from 2.29 in control to 1.14 nmoles/mg protein in thyroxine injected pups. These observations indicate that expression of IgG receptor during postnatal development is a hormone regulated process.
Subject(s)
Animals , Base Sequence , Immunoglobulin G/metabolism , Intestines/growth & development , Protein Binding , RNA, Messenger/genetics , Rats , Rats, Wistar , Receptors, IgG/geneticsABSTRACT
The effect of chronic ethanol feeding has been studied on intestinal alkaline phosphatase (IAP) activity. The enzyme was assayed using p-nitrophenyl phosphate (PNPP), phenylphosphate (PhP) and beta-glycerophosphate (beta GP) as the substrates. Feeding of ethanol for 10 days did not effect the enzyme activity but it was markedly elevated in animals fed ethanol for 20 or 30 days. However, ethanol administration to rats, for over 6 wk exhibited a decline in IAP activity, both in the soluble and membrane fractions of intestine. Kinetic studies revealed an enhancement in Vmax with no change in apparent Km after 30 days of ethanol feeding and a decrease in Vmax after 6 wk of ethanol ingestion. These results were confirmed by assaying the enzyme activity in non-denatured polyacrylamide gels using 5-bromo-4-chloro-3-indoly1 phosphate (BCIP) as the substrate. These findings suggest differential changes in IAP activity in response to ethanol feeding in rats.
Subject(s)
Alcoholism/enzymology , Alkaline Phosphatase/drug effects , Animals , Intestines/drug effects , Male , Rats , Rats, WistarABSTRACT
Rotavirus induced diarrhoea was investigated in neonatal mice. Assessment of oxidative/antioxidative profile was the mechanistic approach to study the nature of injury. Neonatal mice (NMRI strain) were infected orally with the homologous strain of (EB) rotavirus (serotype 3). The peak severity of rotavirus infection was attained on the third day post infection. The whole small intestine of neonatal mice on day 3 post infection was homogenized and analysed for oxidative/antioxidative profile. Glutathione and related thiols were significantly declined in rotavirus infected group. Superoxide dismutase, glutathione peroxidase and glutathione-S-transferase (1-chloro 2, 4 dinitrobenzene) activities were also decreased in the rotavirus infected group. The activities of glutathione reductase and glutathione-S-transferase (ethacrynic acid) however were elevated with rotavirus infection in comparison to the control group. Similarly, ADP-FeCI3, NADPH induced lipid peroxidation was elevated with rotavirus infection. Thus the altered oxidative/antioxidative profile indicated the presence of oxidative stress in the rotavirus infected group and can be postulated to have a prominent role in the pathogenesis of the disease.