Search PubMed⌕ Search

Biomedical subjects

B F Trump

Publications and source records attributed to B F Trump.

At least 127 records · Page 7Linked to original sources
PubMed1985

Immunohistochemical studies of keratin in human bronchus and lung tumors.

Lung tumors of various types, fixed in 4% formaldehyde-1% glutaraldehyde, were stained for keratin proteins. The results were compared with previous ultrastructural evidence of intermediate filament bundles (IFBs), presumed to be keratin. Electron and light microscopic methods were largely complimentary and the results were in agreement in 79% of cases. Light microscopy was superior for demonstrating keratinizing foci containing numerous well-developed IFBs, whereas electron microscopy was superior when keratin filaments were sparsely distributed in cells throughout a tumor. Fetal and adult bronchial specimens were also studied. Normal adult bronchus, fixed in aldehydes, was unreactive but keratin was observed in similarly fixed bronchi that showed epidermoid metaplasia and/or intraepithelial carcinoma. Keratin was demonstrated in normal adult bronchi fixed in ethanol. Keratin was not observed in fetal lung until the 14th week of gestation, when it appeared in basal cells and a few columnar cells of the larger bronchi. Thereafter, keratin progressively appeared in the more distal branches. As specimens from gestations of less than 14 weeks were fixed in aldehydes, the apparent lack of immunoreactivity may have been artifactual. Nevertheless, keratin was demonstrable in aldehyde-fixed fetal bronchi at 16 and 23 weeks' gestation.

Adult↗
PubMed1985

In vitro studies of human lung carcinogenesis.

Advances in the methodology to culture normal human lung cells have provided opportunities to investigate fundamental problems in biomedical research, including the mechanism(s) of carcinogenesis. Using the strategy schematically shown in Figure 1, we have initiated studies of the effects of carcinogens on the normal progenitor cells of the human cancers caused by these carcinogens. Extended lifespans and aneuploidy were found after exposure of mesothelial cells to asbestos and bronchial epithelial cells to nickel sulfate. These abnormal cells may be considered to be preneoplastic and at an intermediate position in the multistage process of carcinogenesis. Human bronchial epithelial cells can also be employed to investigate the role of specific oncogenes in carcinogenesis and tumor progression. Using the protoplast fusion method for high frequency gene transfection, vHa-ras oncogene initiates a cascade of events in the normal human bronchial cells leading to their apparent immortality, aneuploidy, and tumorigenicity in athymic nude mice. These results suggest that oncogenes may play an important role in human carcinogenesis.

Animals↗
PubMed1985

Pathophysiology of hemorrhagic shock. A model for studying the effects of acute blood loss in the rat.

A model of acute blood loss in rats with a reproducible mortality rate over a wide range of body weights was developed by withdrawing various amounts of fixed blood volume per 100 g body weight via the left common carotid artery and observing the survival of the animals. Younger (lighter) animals survived the bleeding longer than older (heavier) animals. As early as 70 min following the shock episode there was evidence of acute tubular necrosis in kidney proximal tubules and focal centrilobular necrosis in the liver. The 84%, 50%, or 16% body weight - mortality line was: V84 = -0.17 BW + 3.25; V50 = -0.18 BW + 3.16; or V16 = -0.18 BW + 3.01 in animals ranging from 250 to 400 g body weight (where V = bleeding volume ml/100 g body weight, BW = body weight in grams X 10(-2). To produce the same mortality rate, the bleeding volume per unit body weight decreased with increased body weight. On the other hand, the bleeding volume per total blood volume or per unit body surface area increased with increased body weight. The body weight-mortality line is a useful method to calculate the bleeding volume to produce predetermined mortality rate. This method can be easily applied to various pathophysiological and metabolic studies on the nature of acute blood loss as well as in the treatment of acute blood loss.

Age Factors↗
PubMed1985

Distribution of blood group antigens A, B, H, Lewisa, and Lewisb in human normal, fetal, and malignant colonic tissue.

In humans, most blood group substances (BGS) are expressed throughout the fetal colon but are absent from the distal portion of adult colon. Cancers of the distal colon frequently reexpress BGS thereby suggesting that these antigens behave as oncofetal antigens at this organ site. We used a sensitive immunoperoxidase method with monoclonal antibodies directed against blood groups A, B, O (H), Lewisa and Lewisb to systematically evaluate BGS expression in fetal colon, normal adult colon from immediate autopsies of kidney donors, mucosa adjacent to cancer (transitional mucosa) and colorectal cancer tissues. In normal colon, BG-A, B, H, and Lewisb were expressed in proximal but not distal colon, whereas Lewisa was distributed uniformly throughout the colon. In colon cancer, and fetal colon, the proximal-distal gradient of BG-A, B, H, and Lewisb expression was abolished because of enhanced distal expression of these antigens. In cancer tissues, three patterns of altered BGS expression emerged: (a) incompatible expression of BG-A or BG-B (over 50% of patients); (b) deletion of BGS; and (c) precursor BG-H accumulation (80% of 25 tumors). BGS staining of transitional mucosa closely resembled that of the adjacent tumor except that no examples of BGS deletion were encountered in transitional mucosa. The goblet cell secretory vacuole accounted for most of the BGS expression in normal colon, but cancer cells demonstrated differentiation-dependent antigenic expression such that well-differentiated tumors expressed BGS on cell apical membranes and glandular contents, but poorly differentiated cancers exhibited diffuse cytoplasmic staining. These findings confirm the oncofetal nature of BGS in distal colon cancer, and provide immunohistochemical evidence for a diverse repertoire of altered antigen expression in colon cancer. Further investigation is needed to elucidate the possible genetic and biochemical mechanisms involved.

ABO Blood-Group System↗
PubMed1985

Cis-diamminedichloroplatinum (II)-induced acute renal failure in the rat. Correlation of structural and functional alterations.

Studies were undertaken to examine the relationship between renal morphologic and functional alterations during the development of cis-diamminedichloroplatinum (II) (CDDP)-induced acute renal failure (ARF). Control and CDDP-treated rats (10 mg/kg, intraperitoneally) were housed in metabolic cages for the purpose of renal function determinations. Renal morphology was studied by light and electron microscopy at 6, 24, 48, 72, and 96 hours following treatment. Six hours following CDDP administration, morphologic alterations consisting of nucleolar segregation, ribosome dispersion, and the formation of aggregates of smooth endoplasmic reticulum were observed throughout the P3 portion of the proximal tubule located in the outer stripe of the outer medulla and medullary rays. These changes became more frequently observed throughout P3 during the course of the study. At 24 and 48 hours, focal changes were also observed involving the P1 and P2 segments of the proximal tubule which make up the pars convoluta. ARF, indicated by a reduced creatinine clearance, was first apparent 48 hours following CDDP administration. The development of ARF was associated with focal, primarily sublethal, cell injury throughout the proximal tubule. By 72 and 96 hours necrosis primarily affecting P3 became widespread, and renal function progressively worsened. The establishment of ARF prior to the development of tubular necrosis suggests that the processes of tubular obstruction and/or tubular fluid backleak are not involved in the initiation of ARF in this model. Instead, the alterations involving P1 and P2 appear to be most important during the early stages of CDDP-induced ARF. The severity of the convoluted tubular injury at 48 hours showed a significant correlation with the degree of renal function impairment. The tubular injury affecting P3 did not correlate with the loss of renal function at any of the time points studied. However, tubular injury in P3 did appear responsible for some degree of renal function impairment at 72 and 96 hours, probably as a result of tubular obstruction and/or tubular fluid backleak.

Acute Kidney Injury↗
PubMed1984

Unbuffered osmium staining of cell organelles: alterations induced by cell injury.

We have studied the localization of osmium reduction products to investigate the functional state of organelles as well as organelle interrelationships during cell injury. In normal hepatocytes osmium deposits of variable intensity are seen in nuclear envelope, endoplasmic reticulum. Golgi cisternae and vesicles and lysosomes. Buffering of osmium with s- collidine (pH 7.4) prevents the deposition of osmium. Reversible (30 min) and irreversible (60 min) ischemia without reflow causes no change in the pattern of osmium deposition. Irreversible ischemia followed by reflow causes decreased staining of endoplasmic reticulum (ER) and redistribution of the osmium deposits through the cytoplasm. Reversibly injured pancreatic acinar cells in cultured explants manifest a similar loss of osmium staining in the endoplasmic reticulum cisternae. The administration of antimicrotubule drugs induces an accentuation of osmium staining in localized cisternal elements of hepatocytes. These heavily stained cisternae appear to give rise to the bounding membranes of drug-induced autophagic vacuoles. Cytoplasmic organelles sequestered inside the autophagic vacuoles acquire intense staining when they begin to undergo degradation. In homogenized liver tissue all the subcellular organelles show osmium deposits. The deposits are preferentially localized along the organelle membranes. In particular the dense deposits in the ER lumen are not seen in the subcellular fractions. Phospholipase A2 (3 units/mg protein) enhances the deposition of osmium in the lumen of microsomal vesicles, whereas the presence of detergent has no such effect. Addition of EDTA to the homogenizing medium enhances the ultrastructural preservation of the subcellular fractions but has little effect on the deposition of osmium. OsO4 deposition occurs at acid pH and the intensity and pattern of the stain can be modified in vivo and in vitro. Osmium tetroxide deposition is induced at sites of membrane transformation (autophagic vacuoles) and degradation (lysosomes). Calcium influx and phospholipase activation (ischemia, tissue homogenization, phospholipase addition) enhance osmium deposition and/or influence the localization of the staining pattern.

Animals↗
PubMed1984

Metabolic studies of postischemic acute renal failure in the rat.

Postischemic acute renal failure was induced by 1 hr of clamping of the renal vasculature. Adenine nucleotide (ATP, ADP, AMP) and lactate (Lac) levels were measured after 0, 0.25, 1, 6, 24, and 48 hr of reflow to determine the time necessary for recovery to control levels. After 1 hr of ischemia with no reflow, [ATP] was 18% and [Lac] was 10-fold control levels. Control levels were restored after 24 hr of reflow. Variable ischemic times (5, 15, 30, 60, 90, and 120 min) followed by (1) no reflow or (2) 24 hr of reflow were also studied. [ATP] decreased to 25 and 13% of controls after 5 and 120 min of ischemia, respectively, and [Lac] increased to 5- and 13-fold controls after 5 and 120 min. Five to ninety minutes of ischemia followed by 24 hr of reflow resulted in a trend toward restoration of ATP and Lac levels; whereas, 120 min of ischemia followed by 24 hr of reflow resulted in death. The results indicate that: (1) In vivo ischemia results in a drastic and rapid shift in the ATP-ADP-AMP equilibrium; (2) the absolute concentration of ATP is not a reliable criterion of cell viability, but the ability to resynthesize ATP may be determinant in the reversibility of the lesion; (3) 1 hr of ischemia is reversible with respect to restoration of [ATP] and [Lac], but 24 hr of reflow are needed for restoration; and (4) ischemia for 90 min results in a metabolic derangement which is partially reversible in that metabolite levels are partially restored after 24 hr of reflow. However, 90 min of vascular clamping is not functionally reversible since the majority of animals exhibit severe azotemia and do not survive.

Acute Kidney Injury↗
PubMed1984

Carcinogen induced unscheduled DNA synthesis in mouse hepatocytes.

Mouse primary liver cell cultures were examined for evidence of unscheduled DNA synthesis (UDS) following treatment with the carcinogens; dimethylnitrosamine (DMNA), diethylnitrosamine (DENA), 2-acetylaminofluorene (2-AAF), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), benzo(a)pyrene (BP), dimethylbenzanthracene (DMBA), 1,1,-bis(p-chlorophenyl)-2,2,2-trichloroethane (DDT), safrole, diethylstilbestrol (DES), aflatoxin B1 (AFB1), and dieldrin and the noncarcinogens; dimethylformamide (DMF), fluorene, and pyrene. Mouse hepatocyte cultures were simultaneously treated with three concentrations of each compound and 3H-thymidine. After 24 hrs, cells were fixed and processed for autoradiography. 3H-thymidine incorporation in both experimental and control cell nuclei, as evidenced by autoradiographic grains, was quantitated microscopically. DMNA, DENA, 2-AAF, MNNG, BP, AFB1 and DMBA significantly increased UDS over untreated cells at all concentrations studied. DDT, DMF, fluorene, pyrene, safrole, DES, and dieldrin were negative for UDS in all concentrations examined. DMNA, 2-AAF and MNNG were also studied for UDS induction in 2 hr old, 1 day old and 4 day old cultures. A progressive decrease in UDS with increased time after plating was found in DMNA and 2-AAF treated cultures. After 4 days DMNA and 2-AAF induced UDS only at the highest concentrations examined (10(-3) M and 10(-4) M respectively). MNNG induced UDS at all time periods and concentrations sampled. An attempt to enhance the sensitivity of the UDS assay by inducing the mixed function oxidative enzyme activity in the hepatocytes with phenobarbital administered in vivo resulted in no statistically significant increase in UDS with DMNA, 2-AAF, MNNG, DDT, and dieldrin when compared with cells from non-induced animals.

Animals↗
PubMed1984

Protection of hepatocytes with hyperoxia against carbon tetrachloride-induced injury.

Hyperbaric oxygen (HPO) was administered to rats (100% O2 at 2.8 atm for 90 min) immediately or 1 hr after severe carbon tetrachloride (CCl4) intoxication in order to study the mechanisms of protection against hepatocellular injury by hyperoxia. Slight to moderate hepatocellular injury was observed, particularly by morphologic criteria, 4 hr after CCl4 intoxication. Little cell death was observed; 24 hr after CCl4, 20% of the untreated animals died. In the survivors, the following typical changes occurred in the liver: extensive hepatocellular swelling, vacuolization and necrosis; severe ultrastructural alterations; binding of CCl4 to microsomal lipids; elevation of lipid peroxidation products (conjugated dienes); little decrease in cytochrome b5 and severe decrease in cytochrome P-450 levels. Serum transaminase (alanine aminotransferase and aspartate aminotransferase) levels were elevated. Immediate treatment with HPO prevented the mortality and markedly decreased the hepatocellular necrosis 24 hr after intoxication. Immediate HPO treatment did not lower the levels of free CCl4 in the liver. However, the rise in lipid peroxidation products caused by CCl4 intoxication at 4 hr was reduced. Delayed treatment with HPO (1 hr after CCl4) prevented the mortality but was less effective in preventing necrosis. Some hepatocellular protection was still demonstrable. In particular, the rise in lipid peroxidation products was reduced. Hyperoxia protects hepatocytes against CCl4 toxicity. The rapid decline in protective effect within 60 min of intoxication suggests that hyperoxia inhibits CCl4 activation and/or damage from molecular intermediates. Hyperoxia has little effect on the progression of sublethal injury to cell death in the livers of CCl4-intoxicated rats.

Alanine Transaminase↗
PubMed1984

Chemical carcinogenesis in the tracheobronchial epithelium.

Some of the recent work in pulmonary carcinogenesis is briefly reviewed. Morphologic studies of neoplastic and preneoplastic lesions of the human bronchi are compared with similar studies of carcinogenesis and epithelial regeneration in the hamster trachea. These studies suggest that bronchogenic carcinomas are typically complex mixtures of three basic phenotypes, the epidermoid and the mucous and dense-core granulated (endocrine) phenotypes. Pure forms of these phenotypes are rare, as different cells and even individual cells in single tumors express more than one phenotype. The clinical significance of such phenotypic variability is not yet known. Bronchial cell types which retain the capacity to divide include the mucous cell, the basal cell and perhaps the dense-core granulated cell. Studies of epithelial regeneration and preneoplastic lesions suggest that the mucous cell may be pivotal both in the response to injury and in carcinogenesis. Cigarette smoking is believed to be the major etiologic factor in bronchogenic carcinoma. Cigarette smoke contains initiators of carcinogenesis, but it contains a plethora of probable promoters and cocarcinogens as well. It is hypothesized that cigarette smoke may both initiate bronchial cells and promote carcinogenesis in cells which have previously been initiated by smoke or other factors. It is further hypothesized that that mucous cell is the major target for initiation and subsequent tumorigenesis. The ultimate phenotype(s) displayed by the tumor is suggested to result from the effect of microenvironmental factors upon the initiated cell and its progeny.

Animals↗
PubMed1984

Cell calcium, cell injury and cell death.

The role of calcium in cell injury has been the subject of much recent investigation. The movement and redistribution of this cation from extra to intracellular compartments and the calcium shifts between intracellular compartments may well play a determinate role in the cell's reaction to injury. Therefore, data of such shifts and their correlation with morphological, biochemical and cytoskeletal studies will provide a better understanding of these processes. To study the effects of calcium regulation on acute lethal anoxic injury and the effects of inhibition of respiration with cyanide, three experimental systems were utilized: Ehrlich ascites tumor cells, isolated rabbit proximal tubule segments and suspended or cultured rat proximal tubule cells. Although our data showed no correlation between total cell calcium and cell death except in highly selected cell systems, they did indicate that calcium can be an important control variable. Therefore, massive increases in total cell calcium, as seen in Ca3(PO4)2 precipitation in mitochondria, must be a secondary event and represent the modern day equivalent of the classical dystrophic calcification seen by pathologists in the past. Although the involvement of extracellular calcium in cell death may well be significant in some cell types, redistribution of calcium within the intracellular compartments may play an even more important role.

Adenosine Triphosphate↗
PubMed1984

Immunocytochemical evaluation of human prostatic carcinomas for carcinoembryonic antigen, nonspecific cross-reacting antigen, beta-chorionic gonadotrophin, and prostate-specific antigen.

The unlabeled antibody peroxidase-antiperoxidase technique was used to examine human malignant prostatic tissue (primary tumors) for the presence of prostate-specific antigen (PSA), carcinoembryonic antigen (CEA), nonspecific cross-reacting antigen (NCA), and beta-chorionic gonadotrophin (HCG). The results were compared to those obtained with normal and hyperplastic prostate tissue (BPH). All specimens of neoplastic, hyperplastic, and normal prostate tissue showed immunostaining reactions for PSA. Immunostaining for PSA was relatively uniform among samples of normal and BPH tissue, but variations with respect to intensity of PSA immunostaining were noted among prostate tumors as well as between the neoplastic cells of individual tumors. Some areas of normal or hyperplastic prostatic epithelium within tumors showed stronger staining reactions for PSA than the tumor cells themselves. Using an antiserum which was able to detect both NCA and CEA, it was found that 16 of 38 tumors (42%) had positive immunostaining reactions. Of these, 15 were subsequently shown to contain only NCA immunoreactivity, and 1 tumor had both NCA and CEA immunoreactivity. NCA, but not CEA, immunoreactivity was identified in hyperplastic prostate tissue within tumor specimens and in BPH specimens. Neither antigen was detected in normal prostatic epithelium. Three of 38 tumors (8%) were found to contain neoplastic cells with HCG immunoreactivity. HCG immunoreactivity was not identified in BPH or normal prostatic tissue. Therefore, HCG and CEA immunoreactivity appear to be tumor-associated antigens in prostate cancer which are expressed with a low incidence. The results of the study identified prostate tumors with different patterns of immunocytochemical markers: 22 of 38 tumors (58%) contained only PSA immunoreactivity; 13 of 38 tumors (34%) contained PSA and NCA immunoreactivity; 2 of 38 tumors (5%) were positive for PSA, NCA, and HCG immunoreactivity; and 1 of 38 tumors (3%) contained PSA, NCA, HCG, and CEA immunoreactivity. Apart from PSA, which was present in all tumors, the markers studied here appeared to be more frequently expressed in well-differentiated tumors than in less-differentiated tumors. Our results suggest the possibility of subclassifying prostate tumors by means of immunocytochemistry.

Antigens↗
PubMed1984

Keratin proteins in human lung carcinomas. Combined use of morphology, keratin immunocytochemistry, and keratin immunoprecipitation.

Light-microscopic immunocytochemistry and electron microscopy demonstrated that adenocarcinomas (AC) and squamous cell (epidermoid) carcinomas (SCCs) of human lung contained keratin proteins in the form of tonofilament bundles. However, moderately differentiated (md) SCCs contained abundant keratin, whereas poorly differentiated (pd) SCCs and all ACs contained lesser amounts. Lung tumors with the diagnosis of AC or SCC, as defined by WHO criteria, were also analyzed by immunoprecipitation techniques for the presence of keratin proteins. Regardless of the degree of tumor differentiation, SCCs contained a 44 kd keratin which was lacking in ACs. Interestingly, normal bronchial epithelium also contained the same 44 kd keratin. In addition, as SCCs became more differentiated, they exhibited even greater differences in the profile of synthesized keratins. Specifically, the relative abundance of the intermediate-sized keratins (57 and 59 kd) was increased in the md SCCs. Although keratin protein patterns appear to be a valuable adjunct in distinguishing AC from SCC, their usefulness as a diagnostic tool will require survey of a larger number of poorly differentiated tumors.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed1984

Degradation of zymogen granules by lysosomes in cultured pancreatic explants.

Pancreatic explants from Syrian hamsters were maintained in culture for determination of the fate of the zymogen granules in the acinar cells. By 6 hours of culture the zymogen granule matrix in many cells becomes nonhomogeneous, and electron-lucent spaces appear. Autoradiography performed 48 hours after pulse labeling shows that several of the altered zymogen granules contain radioactively labeled proteins. Hence these altered granules are mature zymogen granules undergoing regression. Ultrastructural analyses indicate that the zymogen granules are degraded intracellularly in the lysosomes by autophagy, by direct fusion between the lysosomes and the zymogen granules, as well as by engulfment of intact zymogen granules by the lysosomes. Budding of cytoplasm into zymogen granules is also frequently observed. Acid phosphatase histochemistry and anti-amylase immunohistochemistry were used for demonstration of presence of hydrolases and of secretory material in the degenerating zymogen granules. Cycloheximide and low temperature inhibit the degradation of zymogen granules and enhance the short-term viability of the explant. Secretagogues stimulate secretion but have little or no effect on the degradation of zymogen granules or on explant viability. The lysosomes participate in the intracellular degradation of zymogen granules in acinar cells of pancreatic explants. The induction of these lysosomal catabolic processes correlates with the structural alteration of pancreatic acinar cells. The intracellular degradation of secretory membranes and products by the lysosomes may play a role in the adaptation of pancreatic acinar cells to injury.

Acid Phosphatase↗
PubMed1984

Hepatic and systemic metabolic responses to aerobic and anaerobic intra-abdominal abscesses in a highly reproducible chronic rat model.

A single, uniform abscess was formed in 100% of the animals inoculated with a fecal pellet made of sterile rat feces, agar, and a known number and strain of bacteria. The effects of monoclonal Escherichia coli abscess (83 rats) were compared to those of sterile abscess (34 rats) and sham operation (35 rats without abscess). Bacteroides fragilis was added to the sterile pellet to study the effect of an anaerobic monoclonal abscess (16 rats) or of a biclonal abscess containing both aerobes and anaerobes (32 rats). After inoculation, a peritonitis stage with leucopenia, hypoglycemia, body weight loss, and slight fever was followed by the abscess stage with leucocytosis and a slight hyperglycemia. Mild hepatic energy charge deficiency and hepatic lactic acidosis were observed in sterile abscess rats, and slightly enhanced energy charge was seen in monoclonal E. coli abscess rats. The addition of B. fragilis to the sterile pellet, alone or together with E. coli, produced hepatic energy charge deficiency and hepatic lactic acidosis, which were significantly enhanced compared with the monoclonal E. coli abscess rats. The greatest effect was seen in the biclonal E. coli plus B. fragilis abscess, suggesting that anaerobic or combined aerobe and anaerobe abscesses may produce a greater hepatic injury than an aerobic organism abscess alone. This may account for the apparent synergic interaction between aerobic and anaerobic organisms.

Abdomen↗
PubMed1984

O6-alkylguanine-DNA alkyltransferase activity in normal human tissues and cells.

Normal adult human tissues and cultured bronchial epithelial cells and fibroblasts exhibit O6-alkylguanine-DNA alkyltransferase activity in vitro by catalyzing the repair of the promutagenic alkylation lesion O6-methylguanine from DNA. The amount repaired by extracts of liver, peripheral lung, and colon extracts was proportional to the amount of extract protein. Repair of O6-methylguanine led to stoichiometric regeneration of guanine in the DNA and stoichiometric formation of S-methylcysteine in protein. Alkyltransferase activity varies in the different human tissues tested in the decreasing order of liver greater than colon greater than esophagus greater than peripheral lung greater than brain. Extracts of lung tissues, cultured human bronchial epithelial cells, and fibroblasts had similar alkyltransferase activities. Various human tissues exhibit 2- to 10-fold higher alkyltransferase activity than corresponding rat tissues. Whereas the interindividual variation of the activity was 4- to 5-fold in ten or more human lung and colon specimens, the interindividual variation in the inbred rat was less than 20%. The present results show that different human tissues and cells have a several-fold higher capacity to repair O6-methylguanine in DNA than do rat tissues and that the repair process occurs via a mechanism similar to that shown previously in other mammalian cells and Escherichia coli.

Adult↗