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D F Birt

Publications and source records attributed to D F Birt.

At least 73 records · Page 4Linked to original sources
PubMed1987

Enhanced pancreatic and skin tumorigenesis in cabbage-fed hamsters and mice.

Studies were conducted to evaluate the ability of dietary dried cabbage supplements to inhibit pancreatic carcinogenesis in hamsters and skin tumorigenesis in mice. Pancreatic cancer was induced by treatment with 40 mg/kg body wt N-nitrosobis-(2-oxopropyl)amine (BOP). Cabbage was fed from before carcinogen treatment in low fat diet and, beginning 1 week after BOP treatment, cabbage was given in low fat and high fat diets in comparison with the respective non-cabbage-containing diets. Dried cabbage was incorporated at 9 and 11% levels into the low and high fat diets. Feeding cabbage in the high fat diet elevated the yield of BOP-induced pancreatic ductular carcinoma (1.6 carcinomas/effective animal) in comparison with that observed in hamsters fed cabbage in a low fat diet or in those given a high fat diet without cabbage, 0.6-0.8 carcinomas/effective animal (P less than 0.05). Furthermore, the incidence of BOP-induced gall bladder adenocarcinoma was elevated in cabbage-fed hamsters irrespective of dietary fat intake. Effects of dietary fat and cabbage on food consumption, body weight, and serum T3 and T4 values are described. Skin tumorigenesis was induced in SENCAR mice by 10 nmol 7,12 dimethylbenz[a]anthracene (DMBA) and promoted beginning 1 week later with twice weekly applications of 2 micrograms 12-O-tetradecanoyl-13-phorbol acetate (TPA). Dried cabbage was incorporated into AIN semi-purified diets from before DMBA treatment and throughout TPA treatment. Skin papilloma yield was elevated in DMBA-initiated TPA-promoted mice that were fed diets containing 10% cabbage. Mice fed cabbage developed an average of 8.45 papillomas per mouse following 22 weeks of promotion while mice given control diet developed 7.25 papillomas per mouse (P less than 0.001). Cabbage feeding did not influence survival, food consumption or body weight of the mice. These results suggest the need for further research on the use of cabbage as a chemopreventive measure.

Animals↗
PubMed1987

Differential effects of dietary selenium on hepatic and renal glutathione-related enzymes and on hepatic microsomal drug metabolism in the rat.

These studies were undertaken to assess the effect of dietary selenium on glutathione-related enzyme activities in the liver and kidney and on hepatic drug metabolism. The intent was to study underlying mechanisms of selenium-induced beneficial effects in some models of hepatoxicity and carcinogenesis. Dietary selenium, as sodium selenite, was incorporated into a torula yeast basal diet (0.02 ppm selenium) and fed to male rats at supplementation levels of 0.0-5.0 ppm selenium for periods of three or six weeks. Additionally, a commercial cereal-based diet (CD, 0.05-0.08 ppm selenium) was compared to the experimentally defined diet (DD) supplemented with approximately the same amount of selenium. Liver and kidney glutathione peroxidase activity essentially plateaued at levels of selenium of 0.1 ppm and greater. CD- and DD-fed animals had hepatic and renal glutathione peroxidase activities which were similar. Glutathione S-transferase activity in liver, but not kidney, increased with increasing supplements of selenium. Glutathione S-transferase activities in CD- and DD-fed rats were not different. Cytochrome P-450 content and associated oxidative drug metabolism activities were relatively unmodified by selenium. Overall, dietary selenium appeared to act by enhancing potential conjugative detoxication pathway, rather than by decreasing the potential activation of chemicals via the hepatic cytochrome P-450 system.

Animals↗
PubMed1986

Dietary fat and experimental carcinogenesis: a summary of recent in vivo studies.

Diets high in fat have been demonstrated to enhance carcinogenesis in numerous models. Studies on the relationship between dietary fat and cancer in experimental animals have improved with the evolution in our knowledge of the carcinogenic process and with our ability to formulate better controlled diets. This paper summarizes studies conducted during the past 15-20 years on the effects of dietary fat on in vivo carcinogenesis. Relationships between skin carcinogenesis and dietary fat have received little attention during this time, but tremendous progress has been made in our understanding of mammary and colon carcinogenesis. Studies have been conducted of mammary carcinogenesis induced in various rat strains by several chemical carcinogens or by X-irradiation. Several colon carcinogenesis models have also been used to evaluate dietary fat effects. Recent studies in the lung, liver, and pancreas have shown relationships between the carcinogenic process at these sites and dietary fat; however, further studies are needed. The confounding between high fat intakes and low carbohydrate intakes and the difficulties of separating high fat intake from high caloric intake must be addressed in future research. The mechanism of the observed effects of dietary fat is unknown.

Animals↗
PubMed1986

Dietary fat and selenium effects on ex vivo prostaglandin production in rat colon, kidney, and blood.

The effects were determined of dietary fat and selenium (Se) levels on prostaglandin (PG) production in rat blood, kidney, and colon mucosa. For 30 weeks, male Wistar-derived MRC rats were prefed diets containing low (6 g/367 kcal) or high (20 g/367 kcal) levels of fat with one of three Se supplements from sodium selenite: 0.0, 0.1, or 2.0 ppm Se. PG production was stopped by adding aspirin immediately following removal of the blood, kidney, and colon samples. Separate samples were allowed to incubate 10 or 60 minutes before blockage of PG production for determination of ex vivo PG production. Prostaglandin E2 (PGE2), thromboxane B2, and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured by radioimmunoassay following separation on silicic acid columns. Basal levels of the three PGs were not influenced by diet. PGE2 production in the colon was highest in the group fed the high-fat diet that contained 2.0 ppm Se at 10 and 60 minutes, but PGE2 production in the blood and kidney were not altered by diet. Thromboxane B2 production in the rats' blood was higher in those prefed high-fat diets, but it was not influenced by dietary Se. Production of 6-keto-PGF1 alpha in the blood and thromboxane B2 and 6-keto-PGF1 alpha production by the kidney and colonic mucosa were not influenced by either dietary fat or Se.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Anti-mutagenesis and anti-promotion by apigenin, robinetin and indole-3-carbinol.

We assessed the anti-mutagenic and anti-promotion properties of two flavones, apigenin and robinetin, and of indole-3-carbinol, because these compounds have been reported in vegetables, the consumption of which has been associated with reduced rates of cancer. However, the active components of these foods and their effects on carcinogenesis have not been established. Anti-mutagenicity was determined in the Salmonella typhimurium assay by measuring the effects of the test compounds on bacterial mutagenesis induced by methyl-nitrosourea (MNU), methyl-n-nitro-N-nitrosoguanidine (MNNG), benzo[a]pyrene (BaP) or 2-aminoanthracene (2-AA). Inclusion of apigenin resulted in a 62% and a 43% inhibition of mutagenicity with 13 nmol of 2-AA and 30 nmol BaP respectively. Robinetin caused an 87% inhibition of mutagenicity by 2-AA, but indole-3-carbinol had little or no effect on the mutagenicity of any of the compounds. None of the three compounds inhibited mutagenesis by MNU or MNNG and none were mutagenic or toxic when tested in the absence of mutagenic compounds at doses up to 20 micrograms/plate. Anti-promotion properties were assessed by measuring the effects of apigenin, robinetin and indole-3-carbinol on induction of ornithine decarboxylase activity (ODC) in mouse epidermis by 17 nmol 12-O-tetradecanoyl phorbol-13-acetate (TPA). Pretreatment of the skin half an hour before TPA with apigenin, robinetin, butylated hydroxyanisole, 13-cis-retinoic acid (all at 50 mumol) or di-fluoromethylornithine (1.6 mumol) inhibited ODC induction at 6 h after TPA by 67-80%. Pretreatment with 50 mumol indole-3-carbinol caused a 78% elevation in the TPA induction at this time. Dose response measurements were conducted with apigenin, indole-3-carbinol and robinetin. Inhibition by 30-90% of TPA-induced ODC was observed at 6 h after TPA in mice pretreated with 12.5-100 mumol apigenin. Pretreatment with 37.5 or 50 mumol indole-3-carbinol or 0.5, 12.5 or 25 mumol robinetin resulted in elevated induction of epidermal ODC by TPA at 6 h after TPA. However, treatment with 50 or 100 mumol robinetin diminished ODC induction at 6 h after TPA. Treatment with 100 mumol apigenin or 50 or 100 mumol indole-3-carbinol in non-TPA-treated mouse skin caused elevations in epidermal ODC. In comparing the time course of ODC induction, indole-3-carbinol (50 mumol) pretreatment shifted the induction of epidermal ODC to earlier times, in addition to elevating ODC induction by TPA.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Acetylaminofluorene↗
PubMed1986

Tolerance of low and high dietary selenium throughout the life span of Syrian hamsters.

In lifetime studies on the effects of dietary selenium (Se) levels, Syrian hamsters were fed diets containing low (unsupplemented torula yeast), adequate (0.1 ppm Se supplemented from sodium selenite), or excessive (5 ppm Se supplemented from sodium selenite) levels of Se. A commercial ration was fed to separate groups. Male and female hamsters were assigned to each diet, and blood samples were collected at 54 and 79 weeks of age for determination of Se status. Body weights of male hamsters were generally highest in those fed unsupplemented diets and lowest in those fed 5 ppm Se supplements. Female weights did not differ between the three semipurified diets. Erythrocyte and plasma glutathione peroxidase and blood Se values increased with the increments in dietary Se at the 54- and 79-week measurements. Survival was approximately 40-45% lower in hamsters fed the commercial ration than in those fed semipurified diets, but was not altered by the Se level in the semipurified diet.

Animals↗
PubMed1986

Update on the effects of vitamins A, C, and E and selenium on carcinogenesis.

The effects of vitamins A, C, and E and of selenium on carcinogenesis are briefly summarized and updated. These vitamins and minerals were selected because they have been studied extensively in recent years with a variety of carcinogenesis models. The consumption of vitamin A and its precursors (carotenoids) has been negatively correlated with cancer at a number of sites, particularly the lung. Animal investigations on vitamin A involvement in carcinogenesis have generally been of three types: those assessing the effect of vitamin A deficiency, the effect of excess vitamin A, or the effect of supplementation with synthetic analogs of vitamin A. Vitamin A deficiency had no effect on salivary gland carcinogenesis, enhanced urinary bladder, lung, and liver carcinogenesis, and inhibited colon carcinogenesis. Excess of various forms of vitamin A enhanced or inhibited skin tumorigenesis, inhibited mammary carcinogenesis in rats (but not in mice), and carcinogenesis of the forestomach, liver, and urinary bladder (with one model, but not with another), or enhanced or did not influence lung carcinogenesis. Vitamin A analogs have enhanced or inhibited skin tumorigenesis, inhibited salivary gland, mammary, and urinary bladder carcinogenesis, enhanced tracheal and liver carcinogenesis, and either enhanced or inhibited pancreas carcinogenesis, depending upon the model employed. Although retinoids have been shown to inhibit carcinogenesis at many sites, numerous negative studies have been reported and some reports have indicated enhanced carcinogenesis. The most convincing evidence for the involvement of vitamin C in cancer prevention is the ability of ascorbic acid to prevent formation of nitrosamine and of other N-nitroso compounds. In addition vitamin C supplementation was shown to inhibit skin, nose, tracheal, lung, and kidney carcinogenesis, to either not influence or enhance skin, mammary gland, and colon carcinogenesis, and to enhance urinary bladder carcinogenesis, when given as sodium ascorbate, but not when given as ascorbic acid. Like vitamin C, vitamin E can inhibit nitrosation. Vitamin E was shown to inhibit skin, cheek pouch, and forestomach carcinogenesis, to enhance or inhibit colon carcinogenesis, and to have no effect on or to inhibit mammary gland carcinogenesis, depending upon the method of vitamin E administration or the level of dietary selenium or dietary fat. Selenium effects on carcinogenesis have been recently reviewed and the present discussion only updates this area by indicating that enhancement of carcinogenesis by dietary selenium supplements has been observed in the liver, pancreas, and skin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Effect of dietary protein on N-nitrosobis(2-oxopropyl)amine-induced carcinogenesis and on spontaneous diseases in Syrian golden hamsters.

For assessment of the effect of dietary protein on spontaneous diseases and on the carcinogenicity of N-nitrosobis(2-oxopropyl)amine [(BOP) CAS: 60599-38-4], Syrian golden hamsters were fed either low protein (LP; 9% casein), medium protein (MP; 18% casein), or high protein (HP; 36% casein) in a diet containing a medium fat (corn oil) level. The experimental design permitted distinguishing between the effects of protein levels on initiation and development of various lesions in hamsters, in comparison with a control group that was given MP diet for life. When fed after BOP treatment, HP diet inhibited, among induced tumors, pulmonary adenomas in males. Among spontaneous diseases, LP diet fed before 8 weeks of age enhanced colitis in both males and females, renal and adrenal gland amyloidosis in males, and gastric vascular calcinosis in males but inhibited liver abscesses and liver cysts in both males and females. When fed after 8 weeks of age, LP diet enhanced gastric and renal vascular calcification and parathyroid gland adenomas in both sexes but inhibited hepatic, renal, and adrenal gland amyloidosis in females and liver abscesses and liver cysts in both males and females. The feeding of HP diet before 8 weeks of age enhanced the development of colitis and adrenal gland lipomatosis in both males and females but inhibited the development of adrenal gland amyloidosis and adrenal cortical cell hyperplasia in males. When fed to hamsters after 8 weeks of age, HP diet increased the incidence of adrenal gland amyloidosis in females and colitis in both males and females but reduced the frequency of liver cysts in both males and females and of adrenal cortical cell hyperplasia in males. The overall data and literature review indicate that the effect of dietary protein on tumorigenesis is tissue, sex, species, and strain related.

Amyloidosis↗
PubMed1986

Effects of dietary selenium on bis(2-oxopropyl)nitrosamine-induced carcinogenesis in Syrian golden hamsters.

In studies designed to determine the influence of dietary Se on pancreatic carcinogenesis, Syrian golden hamsters were fed unsupplemented torula yeast diet or diet supplemented with 0.1 or 5.0 ppm Se, from sodium selenite, starting at 4 weeks of age until the termination of the study. In separate groups, hamsters were given the diet supplemented with 0.1 ppm Se until 5 days after carcinogen treatment. Then they were fed either the unsupplemented diet or the diet supplemented with 5.0 ppm Se until the end of the experiment. N-Nitrosobis(2-oxopropyl)amine (BOP; CAS; 60599-38-4) treatment was given as a single sc injection of 20 mg/kg (body wt) at 8 weeks of age, and surviving hamsters were killed 50 weeks later. As a measure of Se status, glutathione peroxidase (GSHPX) activities were determined in plasma, erythrocytes, and liver. Values were elevated in animals fed higher levels of dietary Se. BOP treatment depressed plasma GSHPX at 24 hours and elevated erythrocyte and liver values at 4 weeks. Pancreatic ductular adenoma yields were inhibited with each elevation of dietary Se in female hamsters fed the diets, both before and after BOP administration, and were further inhibited in females that were fed diets containing 0.1 ppm Se before BOP administration and that were changed to the unsupplemented or 5.0-ppm-supplemented diets after BOP was given. Pancreatic ductular adenoma yields were highest in all male groups given diets of 0.1 ppm Se before BOP administration, irrespective of the Se level after BOP was fed. Adenoma yields in males were lowest in hamsters fed unsupplemented diet, both before and after BOP treatment. Pancreatic carcinoma yields were low and not influenced by dietary Se. The incidence of hepatic necrosis was elevated in BOP-treated hamsters fed the unsupplemented diet, and that of biliary cystic adenomas was highest in the group fed 0.1 ppm Se before and after BOP treatment.

Animals↗
PubMed1985

Comparative studies on the effects of semipurified and commercial diet on longevity and spontaneous and induced lesions in the Syrian golden hamster.

Syrian golden hamsters were fed a semipurified or commercial diet from weaning throughout life. Bis(2-oxopropyl)nitrosamine (BOP) was administered at 8 weeks of age (10 mg/kg body wt, sc). Longevity was improved by 26% and 36% increases in the mean life-spans of male and female hamsters, respectively, fed the semipurified diets. Carcinogen treatment did not alter survival. The age-adjusted occurrence rates of pancreatic ductular proliferation, carcinomas, adenomas, and common duct polyps were higher in hamsters fed commercial diet; this indicates an earlier onset of these BOP-induced lesions in hamsters fed this diet. However, their overall incidences were generally similar when the two diet groups were compared. Acinar cell nodules were observed only in hamsters fed semipurified diets and were elevated in BOP-treated females. The onset of pancreatic ductular proliferation and adenomas, bile duct proliferation, parathyroid hyperplasia, and common duct papillary hyperplasia was earlier in females than in male hamsters, especially in groups fed commercial ration. Generalized vascular calcification was observed at an elevated rate and reached a higher overall incidence in hamsters fed commercial ration. The age-adjusted rate of amyloidosis was high in female hamsters and elevated in groups that consumed the commercial ration. In addition, colitis and islet cell hyperplasia occurred more often and earlier in hamsters fed commercial ration, but gallbladder stones occurred most in animals fed semipurified diet. This paper discusses the possible association between these and other observed lesions and survival.

Adenoma↗
PubMed1985

Dietary selenium, glutathione peroxidase activity, and toxicity of 2,3,7,8-tetrachloro-dibenzo-p-dioxin.

TCDD has been shown to inhibit selenium-dependent glutathione peroxidase activity. The role of selenium in TCDD toxicity is not known. We have therefore examined the effect of TCDD administration on hepatic glutathione peroxidase, aryl hydrocarbon hydroxylase, glutathione reductase, and glutathione S-transferase activities, glutathione content, and lipid peroxidation in rats fed 0, 0.10, and 2.0 ppm dietary selenium. TCDD treatment significantly inhibited selenium-dependent glutathione peroxidase in animals on diets containing 0.10 and 2.0 ppm selenium. The selenium-dependent glutathione peroxidase activities in rats on 0.10 and 2.0 ppm dietary selenium were 8.3-and 4.7-fold greater than in animals fed a diet containing 0 ppm selenium. TCDD administration enhanced hepatic microsomal lipid peroxidation by factors of 4.0, 4.9, and 9.8 in animals fed diets containing 0, 0.10, and 2.0 ppm selenium, respectively. The administration of a lethal dose of TCDD to rats fed diets containing 0, 0.10, and 2.0 ppm selenium resulted in 0, 46, and 7% survival, respectively, after 66 d. Aryl hydrocarbon hydroxylase, glutathione S-transferase, and glutathione reductase activities were induced by TCDD. The results indicate that optimum dietary selenium provides partial protection from the toxic effects of TCDD.

Animals↗
PubMed1985

Effects of the interaction of dietary fat and protein on N-nitrosobis(2-oxopropyl)amine-induced carcinogenesis and spontaneous lesions in Syrian golden hamsters.

Syrian golden hamsters were fed four diets in experiments designed to evaluate the effects of the interaction of dietary fat and protein on carcinogenesis induced by N-nitrosobis(2-oxopropyl)amine [(BOP) CAS: 60599-38-4]. The diets consisted of two levels of dietary fat [4.5 g (low fat, LF) or 18 g (high fat, HF) of corn oil/385 kilocalories (kcal)]. These levels were fed with each of two levels of dietary protein [9 g low-protein (LP) and 36 g high-protein (HP) casein/385 kcal]. The four diets were fed to two separate groups of hamsters at two different periods in their life-span. For testing of the effects of diet on tumor initiation, one group received the diets from 3 to 7 weeks of age. At 8 weeks, they were given injections sc of 10 mg BOP/kg body weight and placed on a control diet [9 g corn oil (medium fat) and 18 g casein (medium protein)/385 kcal]. The other group received control diet until 8 weeks of age, at which time they were given injections of BOP and placed on the four diets. This group was designed to test the effects of the diets on tumor development. BOP-induced lesions in the lungs, liver, common bile duct, gallbladder, and kidneys are described; results in the pancreas were reported separately. In hamsters fed the four diets after BOP treatment, the LF-LP groups had the fewest tumors, the LF-HP-fed and HF-LP-fed groups had intermediate yields of tumors, and the hamsters given HF-HP diet exhibited the largest numbers of neoplasms. Several specific tumor types showed a similar pattern. For example, the pulmonary adenoma incidence, which was low in the non-BOP-treated hamsters, was higher in the HF-HP group than in those fed LF-HP diet after BOP, but it was not influenced by fat at the LP level. In addition, renal adenomas were observed at a low incidence in non-BOP-treated hamsters and in hamsters fed LF-LP levels before or after BOP treatment (0.5% incidence) but were present at an 8% incidence in all other BOP-treated groups. The incidence of biliary cystic adenomas was highest in male hamsters that received HF diets, irrespective of BOP treatment, and BOP treatment resulted in increased yields of this lesion in females only in groups given HF-LP diet.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Interaction of dietary fat and protein in spontaneous diseases of Syrian golden hamsters.

The influence of interactions between dietary fat and protein on spontaneous diseases was investigated in Syrian golden hamsters fed two levels of corn oil [4.5 or 18 g/385 kilocalories (kcal)] with each of two levels of casein (9 or 36 g/385 kcal). The four diets were fed to separate groups in two different sequences: 1) Diets were given during weeks 3-7 and followed by control diet (9 g corn oil and 18 g casein/385 kcal), or 2) control diet was fed during weeks 3-7, and the four diets were fed from week 8 until death. Dietary interactions of fat and protein modified spontaneous degenerative, inflammatory, and proliferative diseases in hamsters. For example, amyloidosis in the liver, kidneys, spleen, and adrenal glands was reduced in females by feeding high-fat-high-protein (HF-HP) diet in comparison with low-fat-high-protein (LF-HP) diet during weeks 3-7 or by feeding LP diets at either fat level after 8 weeks. The incidence of hepatic abscess was highest in males consuming HP diet at either fat level after 8 weeks, and hepatic necrosis was observed most often in hamsters fed HF-HP diet after 8 weeks. Gastric and renal vascular calcification and nephrocalcinosis incidences were reduced by 50-100% in hamsters fed HF-HP diet after 8 weeks, and HF diet fed at this time reduced vascular calcification in the heart in both sexes and in the lungs in males. Inflammation was generally influenced similarly by diets fed either during weeks 3-7 or after 8 weeks. In the prostate gland, inflammation was observed most frequently in males fed HF-LP diet; however, in the vagina inflammation was elevated in females fed HF-HP diet and found in the gallbladder more commonly in hamsters fed HF-HP than in those given LF-HP. The incidence of colitis was decreased by giving HF-LP diet during weeks 3-7 or LF-LP diets after week 8. The incidence of gastric ulcer was high in males fed HF diets during weeks 3-7, and intestinal ulcers were high in those fed LF-LP at this time. The adrenal hyperplasia incidence was highest in males given HF-HP diet before or after 8 weeks and in females given this diet after 8 weeks. Similarly, ovarian and hepatic ductal hyperplasia was highest in females fed HF-HP diet after 8 weeks, and gastric and intestinal hyperplasia increased with the rise in fat at both protein levels in both sexes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animal Feed↗
PubMed1985

Differential effects of dietary selenium on hepatic and renal glutathione metabolism in the rat.

Studies were undertaken to determine whether or not dietary selenium (Se), as sodium selenite, at suboptimal (unsupplemented torula yeast diets, 0.02 ppm Se) or supplemented up to dietary excess, but nontoxic, levels (5.0 ppm Se) could selectively modify hepatic and renal reduced glutathione (GSH) levels and the enzymes involved in GSH metabolism. Male rats were provided torula yeast semipurified diets containing approximately 0.02 ppm Se in the basal diet and supplements of 0.1, 2.0, or 5.0 ppm Se for 3 or 6 weeks. Hepatic GSH increased in a nonlinear manner, with increasing dietary Se at both time points. Renal GSH was not similarly influenced. Neither hepatic nor renal gamma-glutamylcysteine synthetase or gamma-glutamyl transpeptidase activities are altered by supplements of Se. This suggests that synthetic and degradation enzyme activities are not influenced by Se. The capacity for the maintenance of GSH in the reduced state by glutathione reductase activity increased with increasing levels of dietary Se in the liver but not in the kidney. In both tissues greater Se supplements yielded greater tissue burdens of Se. These results suggest that GSH metabolism in hepatic and renal systems is differentially mediated, and the basis for these differences could be influenced by the relative levels in glutathione metabolizing enzymes.

Animals↗
PubMed1984

Direct enzymatic assay for reduced and oxidized glutathione.

A modification of a specific assay for the reduced (GSH) and oxidized (GSSG) species of glutathione is presented and compared with the method of Ellman (1959). The present method has an enzymatic basis using GSH as the specific cosubstrate for glutathione S-transferase activity. The enzymatic method resulted in comparable, but consistently lower, values for GSH and GSSG than did the method of Ellman. The greatest differences between the two methods occurred when measuring renal GSH and GSSG, possibly due to the presence of mixed thiols in the kidney. This enzymatic method was more specific and provided an accurate and reproducible method of GSH and GSSG determination.

Dinitrochlorobenzene↗
PubMed1984

Age effects on hepatic drug metabolism in Syrian hamsters.

The influence of age on hepatic microsomal drug metabolism was determined in male and female Syrian hamsters fed purified diet or commercial ration. Data from hamsters are reported on hepatic contents of microsomal protein and cytochrome P450, as well as activities of arylhydrocarbon hydroxylase and aniline hydroxylase measured at 4, 10, 22, 34, and 64 weeks of age. Hepatic microsomal protein increased at 34 and 64 weeks in hamsters fed purified diet and at 64 weeks in those fed commercial diet. Cytochrome P450 liver content, based on microsomal protein, was highest at 10 weeks in hamsters given purified diets. Peak values were less with the commercial diet and did not differ between 10, 22, and 34 weeks. When expressed on a body weight basis, cytochrome P450 values increased between 4 and 10 weeks in all groups, except in males fed purified diet, in which values increased up to 34 weeks. Arylhydrocarbon hydroxylase activity increased between 4 and 10, 22 or 34 weeks and declined by 64 weeks in every group when based on microsomal protein content or body weight. Aniline hydroxylase activity, based on microsomal protein, increased between 4 and 10 or 22 weeks and then declined by 64 weeks in every group, except in females fed commercial diet, in which no increase occurred. Changes in aniline hydroxylase, based on body weight, were not consistent with these patterns. Maximum values occurred at 4 weeks for females and at 22 weeks for males fed purified diet, but at 10 weeks in males given commercial diet. Declines in drug metabolism between maturity and senescence were greater when data were expressed on the basis of microsomal protein content, when compared with data on a body weight basis.

Age Factors↗