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PubMed2002

Misuse of androgenic-anabolic steroids and human deltoid muscle fibers: differences between polydrug regimens and single drug administration.

The objective of this investigation was to study the effects of androgenic-anabolic steroid (AAS) misuse on deltoid muscle fiber characteristics in experienced, male strength-trained athletes. In a double-blind study, 15 volunteers were administered nandrolone decanoate (ND) for 8 weeks (200 mg/week, intramuscularly). In an additional study, 12 subjects self-administered various AASs at supratherapeutic dosages (AAS group), while 7 non-users served as controls. In all subjects, a percutaneous needle biopsy sample of the deltoid muscle was obtained at baseline and after 8 weeks. Muscle sections were pre-incubated at pH 4.4, stained with adenosine triphosphatase and analyzed morphometrically. In each biopsy sample, at least 150 fibers were classified for "gray level" and "lesser fiber diameter" to determine the mean fiber size, the sizes of type I and type II fibers, and the fiber type distribution. ND administration did not seem to affect any of those parameters. In the AAS group, mean muscle fiber size (+ 12.6%), and the size of type I (+ 10.8%) and type II (+ 14.6%) muscle fibers increased. The fiber type distribution remained unaltered. We conclude that polydrug regimens of AAS misuse at supratherapeutic dosages increased the size of deltoid muscle fibers (especially type II fibers) in experienced strength-trained athletes, while ND at a therapeutic intramuscular dose of 200 mg did not exert any effect.

Adult↗
PubMed2005

Cardiac autonomic dysfunction in rats chronically treated with anabolic steroid.

To date no published data exist regarding the effects of chronic high-dose anabolic-androgenic steroid administration on tonic cardiac autonomic control. The aim of this study was to evaluate, by power spectral analysis of heart rate variability (HRV), the effects of chronic treatment with supraphysiological doses of nandrolone decanoate (DECA) on tonic cardiac autonomic regulation in sedentary rats. Male Wistar rats were treated weekly with 10 mg kg(-1) of DECA (n=7) or vehicle (CONTROL, n=7) for 10 weeks. At the 8th week of treatment, electrocardiogram was recorded in the conscious state, for time- and frequency-domain HRV analysis. Parasympathetic indexes were reduced in DECA group: high-frequency power (CONTROL=11.1+/-3.0 ms2 vs. DECA=3.8+/-0.6 ms2, P<0.05), RMSSD (CONTROL=5.9+/-0.9 ms vs. DECA 3.5+/-0.3 ms; P<0.05) and pNN5 (CONTROL=31.5+/-7.5 ms vs. DECA=13.2+/-2.6 ms; P<0.05). The sympathetic index LF/HF tended to be higher in DECA group (CONTROL=0.65+/-0.15 vs. DECA=1.17+/-0.26, P=0.0546). In conclusion, chronic treatment with DECA, in rats, impairs tonic cardiac autonomic regulation, which may provide a key mechanism for anabolic steroid-induced arrhythmia and sudden cardiac death.

Anabolic Agents↗
PubMed2000

Attenuated beta-adrenoceptor-mediated cardiac contractile responses following androgenic steroid administration to sedentary rats.

Androgenic steroids administered in doses at pharmacological levels to sedentary animals have been shown to result in a reduced beta-adrenoceptor-mediated increase in systolic cardiac performance when assessed in vivo. Whether the attenuated adrenergic response occurs as a consequence of alterations in either cardiac loads, heart rate, modifications in left ventricular (LV) geometry, or a decrease in myocardial contractile performance has not been determined. In this study the effect of chronic administration (over 3 months) of an androgenic steroid (nandrolone decanoate, 5 mg. kg(-1) biweekly) on the response of load-insensitive indices of myocardial contractile function [the slope of the LV systolic stress-strain relationship (LV-E(n)(max), where E(n)(max) is systolic myocardial elastance)] to an adrenergic-inotropic stimulus was examined ex vivo in paced rat hearts. Systolic cardiac performance was assessed at 300 beats. min(-1) in isolated constant flow perfused heart preparations both before and during 10(-8.5) mol. l(-1) isoproterenol (ISO) infusion (approximate concentration of ISO eliciting 50% maximal inotropic response to ISO). Steroid administration resulted in left-shifted LV systolic and diastolic pressure-volume (P-V ) relationships. The leftshifted P-V relationships were attributed, in part, to increased slopes of these relationships. However, the steroid-mediated increment in the slope of the systolic P-V relationship (systolic chamber elastance, E(max)) was not associated with a similar change in LV E(n)(max) [control 19.2 (SEM 2.1) g. cm(-2), steroid 18.3 (SEM 2.4) g. cm(-2)] as determined in the absence of ISO. Isoproterenol infusion resulted in an increase in both E(max) and E(n)(max) in the control rats, without altering systolic performance in the steroid treated rats. Consequently, in the presence of ISO, the steroid treated rats exhibited a similar E(max), but a reduction in E(n)(max) compared to the control rats [control 25.6 (SEM 1.9) g. cm(-2), steroid 18.5 (SEM 1.5) g. cm(-2); P < 0.05]. In conclusion, these results would suggest that chronic high dose androgenic steroid administration produces a decrease in myocardial contractile reserve to beta-adrenoceptor stimulation.

Anabolic Agents↗
PubMed2003

Biosynthesis of medium-chain-length poly(hydroxyalkanoates) with altered composition by mutant hybrid PHA synthases.

Pseudomonas resinovorans harbors two isogenic poly(hydroxyalkanoates) (PHAs) synthase genes ( phaC1(Pre), phaC2(Pre)) responsible for the production of intracellular medium-chain-length (mcl-)PHAs. Sequence analysis showed that the putative gene-products of these genes contain a conserved alpha/beta-hydrolase fold in the carboxy-terminal half of the proteins. Hybrid genes pha7 and pha8 were constructed by exchanging the alpha/beta-hydrolase-fold coding portions of phaC1(Pre) and phaC2(Pre) at the 3' terminal. When grown with decanoate as carbon source, the pha7- or pha8-transformed Escherichia coli LS1298 produced PHAs containing 73-75% beta-hydroxydecanoate (beta-HD) and 25-27% beta-hydroxyoctanoate (beta-HO). Deletion mutants, Delta pha7 and Delta pha8, were isolated during the PCR-based construction of pha7 and pha8, respectively. Cells harboring these mutants produced PHAs containing 55-60 mol% beta-HD and 40-45 mol% beta-HO. These results demonstrate the feasibility of generating active hybrid mcl-PHA synthase genes and their mutants with the potential of producing polymers having a varied repeat-unit composition.

Acyltransferases↗
PubMed2005

The formation of glycerol monodecanoate by a dehydration condensation reaction: increasing the chemical complexity of amphiphiles on the early Earth.

Dehydration/condensation reactions between organic molecules in the prebiotic environment increased the inventory and complexity of organic compounds available for self-assembly into primitive cellular organisms. As a model of such reactions and to demonstrate this principle, we have investigated the esterification reaction between glycerol and decanoic acid that forms glycerol monodecanoate (GMD). This amphiphile enhances robustness of self-assembled membranous structures of carboxylic acids to the potentially disruptive effects of pH, divalent cation binding and osmotic stress. Experimental variables included temperature, water activity and hydrolysis of the resulting ester product, providing insights into the environmental conditions that would favor the formation and stability of this more evolved amphiphile. At temperatures exceeding 50 degrees C, the ester product formed even in the presence of bulk water, suggesting that the reaction occurs at the liquid interface of the two reactants and that the products segregate in the two immiscible layers, thereby reducing hydrolytic back reactions. This implies that esterification reactions were likely to be common in the prebiotic environment as reactants underwent cycles of wetting and drying on rare early landmasses at elevated temperatures.

Chromatography, Thin Layer↗
PubMed1987

Protein binding studies with radiolabeled compounds containing radiochemical impurities. Equilibrium dialysis versus dialysis rate determination.

The influence of radiochemical impurities in dialysis experiments with high-affinity ligands is investigated. Albumin binding of labeled decanoate (97% pure) is studied by two dialysis techniques. It is shown that equilibrium dialysis is very sensitive to the presence of impurities resulting in erroneously low estimates of the binding affinity and in inconsistent results at varying albumin concentrations. Dialysis rate determination (R. Brodersen et al. (1982) Anal. Biochem. 121, 395-408) is less sensitive to impurities.

Decanoic Acids↗
PubMed1980

Lateral and transversal diffusion and phase transitions in erythrocyte membranes. An excimer fluorescence study.

The lateral diffusion of the excimer-forming probe pyrene decanoic acid has been determined in erythrocyte membranes and in vesicles of the lipid extracts. The random walk of the probe molecules is characterized by their jump frequency, nu j, within the lipid matrix. At T = 35 degrees C a value of nu i = 1.6 . 10(8) s-1 is found in erythrocyte membranes. A somewhat slower mobility is determined in vesicles prepared from lipid extracts of the erythrocyte membrane. Depending on structure and change of the lipids we obtain jump frequencies between 0.8 . 10(8) s-1 and 1.5 . 10(8) s-1 at T - 35 degrees C. The results are compared with jump frequencies yielded in model membranes. The mobility of molecules perpendicular to the membrane surface (transversal diffusion) is investigated. Erythrocyte ghosts doped with pyrene phosphatidylcholine were mixed with undoped ghosts in order to study the exchange kinetics of the probe molecule. A fast transfer between the outer layers of the ghost cells tau 1/2 = 1.6 min at T = 37 degrees C) is found. The exchange process between the inner and the outer layer of one erythrocyte ghost (flip-flop process) following this fast transfer occurs with a half-life time value of t 1/2 = 100 min at T = 37 C. The application of excimer-forming probes presumes a fluid state of the membrane. Therefore we investigated the phase transition behaviour using the excimer technique. Beside a thermotropic phase transition at T = 38 degrees C and T = 33 degrees C we observed an additional fluidity change at T = 38 degrees C in erythrocyte ghost. This transition is attached to a separation of the boundary lipid layer from the intrinsic proteins. No lipid phase transition is observed in liposomes from isolated extracts of the erythrocyte membrane with our methods.

Decanoic Acids↗
PubMed1986

In vitro studies on the oxidation of medium-chain dicarboxylic acids in rat liver.

The degradation of medium-chained dicarboxylic (DC) acids was investigated on purified mitochondria and peroxisomes. Intact organelles were incubated with dodecanedioic acid (DC12), suberic acid (DC8) and adipic acid (DC6), and the production of lower-chained DC-acids and of acetyl-CoA + acetyl-carnitine was monitored. It was shown, that intact peroxisomes could beta-oxidize DC12, DC10, and DC8 at least as far as DC6, while intact mitochondria readily beta-oxidized DC12, and DC10 as far as succinic acid. DC8 and DC6 were not oxidized by intact mitochondria when these two acids were presented externally to the intact organelle. When they were formed intramitochondrially from DC12 and DC10, both DC8 and DC6 were, however, to a great extent beta-oxidized as far as succinic acid. The major reason for this difference between mitochondrial oxidation of externally and internally located DC8 and DC6 seems to be an inability to transport these two acids through the mitochondrial membrane. For DC12 and DC10, the mitochondrial transport systems, which were indicated to be identical to the systems used by the corresponding monocarboxylic acids, were found to be rate-limiting in the beta-oxidation of these acids. A contributing factor to the undetectable beta-oxidation of externally located DC8 and DC6 may also be, that the Km values of DC8-CoA (460 +/- 70 mumol/l) and DC6-CoA (980 +/- 90 mumol/l) towards the acyl-CoA dehydrogenases are very high. These results imply that very high concentrations of intermediates are created intramitochondrially during beta-oxidation, concentrations which are probably only formed through formation of DC8-CoA and DC6-CoA from longer DC-acids and not by transport from outside the mitochondria. The data presented thus for the first time give evidence to a pathway for medium-chained monocarboxylic acids (especially lauric acid and decanoic acid) through cytosolic omega-oxidation followed by activation, transport over the mitochondrial membrane and beta-oxidation to succinic acid.

Acetyl Coenzyme A↗
PubMed1989

Metabolism of pyrenedecanoic acid in Epstein-Barr virus-transformed lymphoid cell lines from normal subjects and from a patient with multisystemic lipid storage myopathy.

A lymphoid cell line has been established from a patient with multisystemic lipid storage myopathy and showed a major triacylglycerol storage, whereas the content of other neutral lipids and phospholipids was in the normal range. The metabolism of the triacylglycerols has been investigated in this lymphoid cell line from multisystemic lipid storage myopathy as well as in control cells through pulse-chase experiments using 10-(1-pyrene)decanoic acid (P10), a fluorescent fatty acid derivative, as precursor. After 1 h incubation, the uptake of P10 was not significantly different in multisystemic lipid storage myopathy and control lymphoid cells. The amount of fluorescent lipids synthesized by the lymphoid cells was proportional to the concentration of P10 in the culture medium. After 24 h incubation, at any extracellular concentration of P10, the content of P10-labelled triacylglycerols was much higher in multisystemic lipid storage myopathy cells than in controls. Chase experiments showed an impairment in the rate of degradation of biosynthesized triacylglycerols in multisystemic lipid storage myopathy lymphoblasts compared to controls with time of chase (the ratio P10-triacylglycerols/P10-phospholipids increased in mutant cells while it decreased in normal cells). Elsewhere, no enzyme deficiency of the neutral triacylglycerol lipase activity, has been found in multisystemic lipid storage myopathy lymphoid cells.

Cell Line, Transformed↗
PubMed1991

Inhibition of long-chain acyl-CoA synthetase by the peroxisome proliferator perfluorodecanoic acid in rat hepatocytes.

Perfluorodecanoic acid (PFDA) is a potent peroxisome proliferator and is known to affect hepatic lipid metabolism in rats. The effects of PFDA on fatty acid utilization were examined in isolated rat hepatocyte suspensions and in rat liver mitochondria and microsomes. PFDA inhibited the oxidation of palmitic acid but not octanoic or pyruvic acids when hepatocytes were incubated with 1 mM PFDA. At this PFDA concentration the esterification of palmitic acid into triacylglycerols was also reduced. The activity of long-chain acyl-CoA synthetase (ACS), an enzyme essential for both oxidation and esterification of fatty acids, was reduced in hepatocytes incubated with 1 mM PFDA. Carnitine palmitoyltransferase (CPT), an important enzyme for the oxidation of long-chain fatty acids, was not altered in hepatocytes incubated with this PFDA concentration. In rat liver mitochondria, palmitate oxidation and ACS activity were reduced significantly (P less than 0.01) at a PFDA concentration that had no effect on CPT activity. The inhibition of ACS by PFDA was similar in liver mitochondria and microsome preparations. In mitochondria incubated with PFDA, the inhibition of ACS appears to be noncompetitive for the substrates palmitic acid and CoA. However, the ACS inhibition by PFDA appeared to be competitive for the ATP binding site of the enzyme. Several chain length perfluorinated fatty acids were examined for their ability to inhibit mitochondrial ACS. Short-chain perfluorinated fatty acids (perfluoroproprionic and -butyric acid) did not inhibit ACS activity. However, medium-chain perfluorinated acids (perfluorooctanoic, -ananoic and -decanoic acid) were found to be potent inhibitors of ACS in isolated mitochondria. Whether ACS inhibition is causally related to PFDA-induced peroxisome proliferation and altered lipid metabolism seen in vivo is yet to be determined.

Animals↗
PubMed1989

Perfluorodecanoic acid decreases the enzyme activity and the amount of glutathione S-transferases proteins and mRNAs in vivo.

The effects of the anti-wetting agent perfluoro-n-decanoic acid (PFDA) on various glutathione S-transferase (GST) enzyme activities were studied in vitro and in vivo. In addition the effects of PFDA treatment on the amount of some glutathione S-transferase subunits and their corresponding translatable mRNA were studied in vivo. PFDA like some other peroxisome proliferators was a non-competitive inhibitor of several GST enzyme activities in vitro. In vivo PFDA reduced the enzyme activity towards substrates which are indicative for the Ya, Yb1 and Yb2 subunits of GSTs to a larger extent than the enzyme activity towards the substrate indicative for the Yc subunit. Whereas the reduction of GST enzyme activities by other peroxisome proliferators was shown to be caused by an inhibition of the relevant enzymes in vivo, PFDA was found to decrease the GST enzyme activities at least in part by lowering the amount of the various GST subunits in vivo due to a lowered concentration of translatable mRNA coding for these enzymes. In addition PFDA abolished the inducibility of GST mRNAs by phenobarbital. Thus PFDA might be an interesting tool for mechanistic studies of the control of GST expression in the liver.

Animals↗
PubMed1996

Effect of structurally diverse peroxisome proliferators on rat hepatic sulfotransferase.

Exposure to perfluorocarboxylic acids, pthalate esters, and some hypolipidemic agents results in the proliferation of peroxisomes in the rodent liver. The structural diversity of these compounds suggests mechanistic diversity in their toxicity as well. To establish reliable biomarkers of peroxisome proliferation (PP) in compounds with distinct chemical toxicities, this study investigated the effect of in vivo exposure to perfluoro-n-octanoic acid, perfluoro-n-decanoic acid, di(2-ethylhexyl)phthalate (DEHP) and clofibrate on two-dimensional electrophoretic protein patterns of rat hepatic sulfotransferases, ST1A1, ST1C1 and ST2A1. After exposure to peroxisome proliferative doses, both ST1A1 and ST1C1 abundance in whole liver homogenates was significantly reduced, but only as a result of perfluorocarboxylic and exposure. The well-established PPs, DEHP and clofibrate had no effect on sulfotransferase expression whatsoever. The observed down-regulation of these STs is significant with respect to their normal detoxication activities and its potential correlation to carcinogenesis warrants further study. The present investigation supports previous studies that demonstrate the unique features of perfluorocarboxylic acid toxicity, relative to classic peroxisome proliferators and endorses the continued use of 2D protein-mapping of Sts and other proteins as biomarkers of chemical toxicity.

Amino Acid Sequence↗
PubMed1985

Pharmacokinetics of 19-nortestosterone esters in normal men.

A reliable method for the isolation of 19-nortestosterone (NT), testosterone (T) and dihydrotestosterone (DHT) by high-performance liquid chromatography (HPLC) and quantitation of the individual steroids by radioimmunoassays is described. The method was used to measure serum concentrations of NT, T and DHT in a pharmacokinetic study and in a clinical trial for male fertility control. Following intramuscular injection of either 50 mg 19-nortestosterone-3-(p-hexoxyphenyl)-propionate (NP) or 50 mg 19-nortestosterone-decanoate (ND) serum NT increased rapidly to maximal concentrations of 4.6 +/- 3.2 and 2.0 +/- 1.3 nmol/l (+/-SD), respectively, in the 6 volunteers. The half-life time was 8 days for ND and 21 days for NP. Based on these findings a clinical trial with NP was performed. NP was given to 5 healthy men in doses of 100 mg/week for the first 3 weeks followed by 200 mg/week for 10 further weeks. Serum NT levels increased gradually and maximal concentrations were reached in the 13th treatment week (20.2 +/- 3.4 nmol/l). Measurable amounts of NT were detectable for 19 weeks after the last injection. The study shows that NT accumulates under this treatment regime and wider spacing of the injection intervals may be possible in future trials.

Adult↗
PubMed1986

Liver lesions in BALB/C mice induced by an anabolic androgen (Decadurabolin), with and without pretreatment with diethylnitrosamine.

Male BALB/C mice were treated with the anabolic androgen Decadurabolin (17 beta-hydroxy-19-nor-androst-4-ene-17 beta-n-decanoate) (DecaD) with and without pretreatment with diethylnitrosamine (DEN). Treatment with DEN alone caused development of severe hepatocytic dysplasia in all animals; 11/11 had cystadenomas and 3/11 haemangiomas, both of which were benign. Mice treated with DecaD alone developed only moderate to severe hepatocytic dysplasia. Treatment with DecaD after DEN induced neoplasms in the livers; 15/15 had severe dysplasia; 14/15 had cystadenomas, 2/15 had haemangiomas, and 4/15 developed nodular proliferation. Single hepatomas were seen in 4/15 livers, two of which also had multiple hepatomas. Control animals had normal liver histology. We conclude that DecaD enhances the hepatocarcinogenicity of DEN, especially with respect to neoplastic lesions in hepatocytes.

Anabolic Agents↗
PubMed1994

Anabolic steroid treatment increases myofiber damage in mdx mouse muscular dystrophy.

In order to study whether myofiber size is an important determinant of the severity of dystrophic injury, mdx and control mice were treated with an anabolic steroid, nandrolone decanoate, for 3 weeks. Treatment resulted in a population of significantly smaller fibers in both strains, and was accompanied by an increase in the proportionate area or the number of foci of dystrophic injury in mdx soleus (slow-twitch) or tibialis anterior plus extensor digitorum longus (fast-twitch) muscles, respectively. As well, serum creatine kinase activity was increased in steroid-treated mdx mice. Fiber centronucleation, an index of accumulated injury and repair, in steroid-treated mdx soleus was doubled compared to that observed in soleus muscles from untreated mdx mice. There was no change in the distribution of immunoreactive basic fibroblast growth factor, important in muscle cell proliferation, with the increased damage from treatment. However, presumptive muscle precursor cells (identified by immunoperoxidase histochemistry for neural cell adhesion molecule), appeared to be more abundant in foci of very recent fiber damage in muscles from steroid-treated than untreated mdx mice. Results show that mdx dystrophy is worsened by anabolic steroid treatment, possibly by altered influences on muscle use patterns and muscle precursor fusion, and is not accompanied by an increase in fiber size.

Animals↗
PubMed1994

Hormonal modulation of extinction responses induced by sexual steroid hormones in rats.

A functional interrelation between the nervous and endocrine systems has been established. However, few studies have dealt with the effects of sexual steroids on learning and memory. The aim of this work was to determine whether sexual steroid hormones could modulate the extinction response of a passive avoidance conditioning in rats. Male Wistar rats, randomly assigned to five groups, two controls and three experimental groups, were submitted to a one-trial passive avoidance conditioning and tested for their retention 24 hr after and during 10 weeks. One control group received no treatment at all, the other received vegetable oil, and the three experimental received 20 mg of testosterone enanthate, 0.8 mg estradiol valerate, or 4 mg nandrolone decanoate, respectively. All substances were applied in a 0.3 ml volume, 24 hours before training and before testing for retention each week during 10 weeks. Results indicate that the extinction process is modulated by these hormones, since testosterone and estradiol facilitate extinction, whereas the anabolic androgen produced a resistance to the extinction process.

Anabolic Agents↗
PubMed1990

Collagen synthesis in postmenopausal women during therapy with anabolic steroid or female sex hormones.

The effect of anabolic steroid therapy and estrogen-progestogen substitution therapy on serum concentration of procollagen type III aminoterminal peptide (PIIINP), a measure of collagen synthesis, in postmenopausal women was studied in two double-blind studies: (1) 39 women allocated to treatment with either 50 mg nandrolone decanoate as an intramuscular depot or placebo injections every third week for 1 year, and (2) 40 women allocated to receive either 2 mg 17 beta-estradiol plus 1 mg norethisterone acetate daily or placebo tablets for 1 year. Serum PIIINP was measured every 3 months during the study. Anabolic steroid therapy resulted in a more than 50% increase (P less than .001) in serum PIIINP at 3 months, which thereafter decayed but remained significantly increased throughout the study period. Serum PIIINP showed the same pattern during estrogen-progestogen therapy, but to a lesser degree. We conclude that anabolic steroids stimulate type III collagen synthesis in postmenopausal women, while estrogen-progestogen therapy may have such an effect, but only to a lesser degree.

Aged↗
PubMed1986

Perfluorodecanoic acid inactivation of a channel for 2-aminopurine in the L5178Y cell membrane and recovery of the channel.

Treatment of L5178Y mouse lymphoma cells with perfluoro-n-decanoic acid (PFDA) in growth medium for 24 hr at 30 degrees C produces a dose-dependent inactivation of a channel in the cell membrane. Activity of the channel was estimated from the initial rate of efflux of a fluorescent purine, 2-aminopurine (AP). The L5178Y cells were preloaded with 100 microM AP and excess AP was removed. The preloaded cells were put in a flow system, and AP efflux was estimated continuously at 21 degrees C from the fluorescence emission of AP at 370 nm. The AP channel was markedly inactivated by a treatment with 150 micrograms/ml PFDA for 24 hr at 30 degrees C. There was no significant recovery of AP flux after 3 days at 30 degrees C in fresh growth medium; however, recovery was significant after 6 days. Recovery of activity of the AP channel occurs in 1 day at 37 degrees C. The initial rate of AP efflux for control cells increases with AP concentration; the reaction is not saturated at 1000 microM AP. The efflux of AP was inhibited by the presence of uric acid in the external buffer. An apparent inhibition constant value of 355 microM was determined for urate inhibition of AP efflux. These observations suggest the presence of a urate-sensitive channel for AP in the membrane of L5178Y cells. The channel was inactivated by PFDA under conditions that had no significant effect on cell viability.

2-Aminopurine↗