Showing papers on "7,12-Dimethylbenz[a]anthracene published in 1995"
TL;DR: The results support the conjecture that oxidative events may be involved in what is operationally referred to as the tumor promotion process by 7,12-dimethylbenz[a]anthracene, and are temporally associated with inflammatory responses that include edema and polymorphonuclear leukocyte infiltration.
105 citations
TL;DR: The observation of different mutant frequencies and spectra in treated and control mice demonstrates the utility of this approach in the study of mutagenesis in vivo, and is consistent with the types of DNA damage induced by DMBA.
Abstract: Transgenic mice carrying the bacterial lacl gene in a lambda shuttle vector were used to isolate and characterize background and 7,12-dimethylbenz[a]anthracene (DMBA)-induced mutations in skin Adult male mice were treated once topically with either DMBA or acetone or were left untreated Seven days later, DMBA treatment had significantly increased the mutant frequency in the skin (mean +/- SEM, 36 +/- 3 x 10(-5)) versus in vehicle-treated (64 +/- 12 x 10(-5)) and untreated mice (71 x 10 x 10(-5)) At least 10 mutants from each of three DMBA-treated and three untreated mice were selected for DNA sequence analysis In each case, the entire 1080-bp target gene was sequenced Base-pair substitutions predominated (86 of 96 mutations), although frameshift and deletion mutations were also detected Twelve percent of the mutants carried more than one mutation In controls, the mutations were predominantly GC-->AT transitions (26 of 42), and no AT-->TA transversions were recovered In contrast, in the DMBA-treated mice, AT-->TA transversions represented 42% of the mutations (23 of 54) and GC-->AT transitions accounted for only 11% The AT-->TA transversions occurred mostly at 5'-CA sites This class of mutation has been recovered frequently in ras genes from DMBA-treated mice and probably represents an early event in carcinogenesis (Nelson MA et al, Proc Natl Acad Sci USA 89:6398-6402, 1992) Our present results are consistent with the types of DNA damage induced by DMBA The observation of different mutant frequencies and spectra in treated and control mice demonstrates the utility of this approach in the study of mutagenesis in vivo
54 citations
TL;DR: Genistein and daidzein suppress SCE and possibly DNA adduct formation induced by the known carcinogen, DMBA, and this response to a low dose isoflavone exposure may be partly responsible for the protective effect against endocrine cancers of soya consumption.
52 citations
TL;DR: The data demonstrate that long-term exposure of DMBA-treated female rats increases the growth of mammary tumors in a highly dose-related fashion, and a highly significant linear relation between flux density and increase in tumor incidence at time of autopsy is indicated.
45 citations
TL;DR: The results suggest that this technique using conventional light-induced fluorescence spectroscopy may be useful for early diagnosis of premalignant and malignant lesions of oral cavity.
Abstract: An attempt was made to study whether light-induced fluorescence spectroscopy could be exploited to discriminate premalignant and malignant tissues of hamster buccal pouch carcinogenesis from normal tissues during a 16 week regimen of tri-weekly topical application of 7,12-dimethylbenz[a]anthracene (DMBA) in liquid paraffin. Histologically, the DMBA-treated buccal mucosa showed hyperplastic changes at 4-6 weeks, papillomas at 8-10 weeks, early invasive carcinomas at 11-13 weeks and finally well-differentiated squamous cell carcinomas at 14-16 weeks of treatment. Acetone extracts of these different staged tissues with age matched control tissues were excited at 405 and 420 nm and the emissions were scanned from 430 and 440 to 700 nm respectively. The spectral profiles of control and transformed tissues were found to be different, each displaying their own characteristic prominent maxima and other spectral marks. The spectra of transformed tissues showed characteristic peaks around 620-630 nm which did not appear in control tissues and the fluorescent intensities at 630 nm [FI(630)nm] were significantly increased from early stages onwards when compared to controls. The spectra of DMBA carcinomas developed at the 18th week after withdrawal of DMBA application at the 10th week and carcinoma extract spiked with DMBA confirmed the peak around 620-630 could be attributed only to porphyrin compounds accumulated in transformed tissues. Furthermore, the ratios of FI(520)nm/FI(630)nm of transformed tissues were also significantly decreased when compared to control tissues. This diagnostic test had a very close resemblance with respect to histological studies. These results suggest that this technique using conventional light-induced fluorescence spectroscopy may be useful for early diagnosis of premalignant and malignant lesions of oral cavity.
32 citations
TL;DR: The unexpected wild‐type properties of the 172Arg→Leu mutant p53, including its ability to stimulate apoptosis, make it a possible candidate for use in gene therapy protocols.
Abstract: Murine p53 containing an Arg-->Leu substitution at amino acid 172 possesses many properties characteristic of wild-type p53, including the ability to induce p21/WAF/Cip1 and apoptosis. To determine if p53-dependent apoptosis plays a critical role in mammary tumorigenesis, transgenic mice were generated in which the expression of this mutant p53 protein was targeted to the mammary gland by using the rat whey acidic protein gene promoter. Mice bearing pituitary isografts were treated with 7,12-dimethylbenz[a]anthracene (DMBA) and examined for mammary tumor development. Mice overexpressing the p53 transgene exhibited a statistically significant increase in apoptosis in the mammary gland and a statistically significant decrease in the incidence of DMBA-induced mammary tumors. No difference in tumor incidence was observed in mice without pituitary isografts who were treated with DMBA, because the transgene is not overexpressed in the absence of hormone stimulation provided by the pituitary isograft. The unexpected wild-type properties of the 172Arg-->Leu mutant p53, including its ability to stimulate apoptosis, make it a possible candidate for use in gene therapy protocols.
27 citations
TL;DR: The consistent occurrence of above N-ras mutation in leukemias indicates that it plays an important role in DMBA-leukemogenesis.
26 citations
TL;DR: It is demonstrated that high dietary fat concentration enhances breast carcinogenesis independently of cyclic ovarian function, although the presence of estrogen may be a prerequisite for significant dietary modulation.
Abstract: The relationships between dietary fat concentration (10 or 40% of energy), fat source (corn oil or beef tallow) and estrogen (control, ovariectomy or ovariectomy with estrogen replacement) to 7,12-dimethylbenz(a)anthracene (DMBA)-induced breast carcinogenesis and survival in rats were studied in a 2 x 2 x 3 factorial experiment. Female Sprague-Dawley rats given DMBA (2.5 mg/100 g body wt, intragastric) at 55 d of age were randomly allocated to three groups 48 h later: sham ovariectomy (control), ovariectomy (OVX) or ovariectomy with a subcutaneous estrogen implant (OVX+E). Each group was subdivided into dietary groups fed 10 and 40% of energy as corn oil or beef tallow for 70 wk. OVX+E rats exhibited serum estrogen concentrations in excess of physiologic values. Survival at 70 wk for the 3 hormonal groups was control 51%, OVX 67% and OVX+E 13%. Mortality in controls was doubled by feeding a high fat diet; no diet effect was detected in OVX or OVX+E rats. Palpable tumors developed in 74, 14 and 60% of control, OVX and OVX+E rats, respectively. High fat diets approximately doubled the hazard of developing a palpable tumor. Adenocarcinoma prevalence was 58, 12 and 63% in control, OVX and OVX+E rats, respectively. The odds of having any tumor, an adenocarcinoma or an adenoma were multiplied by 3.6, 2.8 and 2.3, respectively, for rats fed high vs. low fat. Additional studies showed that diet had no effect on serum prolactin or estrogen concentrations or metabolism and clearance of intravenously administered radiolabeled prolactin. We demonstrated that high dietary fat concentration enhances breast carcinogenesis independently of cyclic ovarian function, although the presence of estrogen may be a prerequisite for significant dietary modulation. The effect of fat on breast cancer is not mediated by major changes in systemic prolactin metabolism.
23 citations
TL;DR: Gestational exposure of ICR mice to the environmental contaminant 7,12-dimethylbenz[a]anthracene was used to study the developmental immunotoxicity of this chemical agent and identify changes in immune cell populations that correlate well with inhibition of cell- and humoral-mediated immunity in experimental animals treated with DMBA.
22 citations
TL;DR: It is demonstrated that high dietary RA inhibited skin carcinogenesis in MEZ-promoted mice at the stages of tumor promotion and malignant conversion, while this inhibition occurred only at the malignant Conversion stage in TPA- Promoted mice.
18 citations
TL;DR: The present data show that the new steroidal antiestrogen EM-170 exerts a potent inhibitory effect in vivo on E1-stimulated growth of DMBA-induced mammary tumors, an effect that is in agreement with the marked reduction caused by the same treatment on tumor estradiol (E2) levels in E 1-treated OVX animals.
Abstract: Recently, compounds having pure antiestrogenic activity have become available. In this study, we examined the activity of the new steroidal antiestrogen EM-170 (N-n-butyl, N-methyl-11-(16′α-chloro-3′,17′α-dihydroxy-estra-1′,3′,5′-(10′)-trien-7′α-yl) undecanamide) on the growth of 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary carcinoma stimulated by treatment with estrone (E1), a steroid known to play an important role as precursor of 17β-estradiol (E2), especially in postmenopausal women. Twenty-five days after ovariectomy (OVX), tumor volume in control OVX animals decreased to 51.4 ± 11% of the initial volume; treatment with E1, administered by Silastic implants, stimulated tumor growth to 179 ± 21%. Treatment with the antiestrogen EM-170 at a dose of 200 µg (twice daily) not only completely reversed the stimulatory effect of E1, but also inhibited tumor growth to 30.5 ± 9.6%, an effect that is 41% (P < 0.01 vs OVX control) greater than that of ovariectomy alone. At a relatively low dose of 40 µg (twice daily), 20 days of treatment with EM-170 reversed by 55% the stimulatory effect of E1 (1.0 µg, subcutaneously, twice daily) on tumor growth in OVX animals. On the other hand, the antiestrogen also induced a significant inhibitory effect on 17β-hydroxysteroid dehydrogenase (17β-HSD) activity in the DMBA-induced mammary tumors, an effect that is in agreement with the marked reduction caused by the same treatment on tumor estradiol (E2) levels in E1-treated OVX animals. The present data show that the new steroidal antiestrogen EM-170 exerts a potent inhibitory effectin vivo on E1-stimulated growth of DMBA-induced mammary tumors, an effect that is probably mediated by both its antiestrogenic activity at the receptor level and its inhibitory effect on 17β-HSD, thus inhibiting local E2 formation and facilitating the action of the antiestrogen at the receptor level.
TL;DR: It is shown that in C3H/10T1/2 fibroblasts the environmental carcinogen 7,12‐dimethyl‐benz[a]anthracene (DMBA) stimulated phosphorylation of ethanolamine (Etn) and in these fibro Blasts DMBA also stimulates phosphorylated choline (Cho).
TL;DR: To characterize the role of formation of DMBADE diastereomers in the induction of mutations, postlabeling assays using [35S]phosphorothioate with adduct separation by HPLC and immobilized boronate chromatography analyses were developed to allow separation and quantitation of DNA adducts formed from each stereoisomer of D MBADE.
Abstract: 7,12-Dimethylbenz[a]anthracene (DMBA), one of the most carcinogenic polycyclic aromatic hydrocarbons in rodent bioassays, is metabolically activated in many tissues to "bay-region" DMBA-3,4-diol-1,2-epoxides (DMBADE). Unlike benzo[a]pyrene, for which the high biological activity of the (7R,8S)-diol-(9S,10R)-epoxide has been established, the low chemical stability of anti-DMBADE has made it impossible to evaluate the role of specific stereoisomers in the biological activity of DMBA. In order to characterize the role of formation of DMBADE diastereomers in the induction of mutations, postlabeling assays using [35S]phosphorothioate with adduct separation by HPLC and immobilized boronate chromatography analyses were developed to allow separation and quantitation of DNA adducts formed from each stereoisomer of DMBADE. In DMBA-treated hamster embryo cell cultures, large quantities of three major adducts (anti-DMBADE-deoxyguanosine, anti-DMBADE-deoxyadenosine, and syn-DMBADE-deoxyadenosine) along with five minor adducts were completely resolved and quantitated. The DNA isolated from a human mammary carcinoma MCF-7 cell-mediated V79 cell mutation assay treated with increasing doses of racemic DMBA-3,4-dihydrodiol contained large amounts of two anti-DMBADE-DNA adducts. The anti-DMBADE adducts accounted for more than 90% of the total adducts at all doses. The number of 6-thioguanine-resistant mutants was proportional to the amount of anti-DMBADE-DNA adducts.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: The results of this study indicate that NNN, when combined with subcarcinogenic doses of other strong carcinogens, is a promoter in the development of squamous cell carcinoma and that 4NQO in 0.5% concentration is a stronger carcinogen than 0.1% DMBA.
TL;DR: The results suggest that cold stress may inhibit lung tumours induced by chemicals and cause lung tumour formation in male and female mice exposed to cold stress.
Abstract: The effect of cold stress on lung tumours induced by 7,12-dimethylbenz[a]anthracene (DMBA) was investigated in ICR male and female mice. When mice were exposed to cold stress at 0±1°C for 2 h, three times per week (every other day) for 3 months, the rectal temperatures and hepatic glutathione levels were significantly decreased. On the other hand, when DMBA (10 mg/kg) was subcutaneously injected into neonatal mice, lung tumours were observed in 81.8% of non-stressed mice of both sexes 4 months after injection. However, when mice treated with the same dose of DMBA were exposed to cold stress under the same conditions, lung tumours were observed in 53.3% and 30.3% of the male and female mice 4 months after DMBA injection. In addition, although DMBA (1 mg/kg) caused lung tumours in 20% or 40% of the treated male or female mice 4 months after injection, it did not cause lung tumours in all of the male and female mice exposed to cold stress. These results suggest that cold stress may inhibit lung tumours induced by chemicals.
TL;DR: The results obtained in this study with these differentiated hepatoma lines demonstrate that they are metabolically competent to activate the promutagens 7,12-dimethylbenz[a]anthracene, benzo[ a]pyrene and cyclophosphamide into their biologically active metabolites as measured by micronucleus induction in the authors' experiments.
Abstract: The capability of two rat hepatoma cell lines, H4IIC3/G - and 2sFou, to detect genotoxicity of xenobiotics, was evaluated in a micronucleus assay. In this system, the cells act as the activation source as well as the target cells for the DNA damage. The study was performed using 7,12-dimethylbenz[a]anthracene, benzo[a]pyrene and cyclophosphamide, as pro-mutagens and mitomycin C as a direct acting mutagen. In both cell lines a significant micronucleus induction was observed after exposure to each test compound, starting from 25 nM for 7,12-dimethylbenz[a]anthracene, 8 μM for benzo[a]pyrene, 0.5 mM for cyclophosphamide and 0.4 μM for mitomycin C. A period of 24 h treatment and 48 h growth was sufficient for induction and expression of micronuclei. The two hepatoma lines behave in a similar way with regard to the pro-mutagen activation. The results obtained in this study with these differentiated hepatoma lines demonstrate that they are metabolically competent to activate the promutagens 7,12-dimethylbenz[a]anthracene, benzo[a]pyrene and cyclophosphamide into their biologically active metabolites as measured by micronucleus induction in our experiments. However, the variable dose responses to 7,12-dimethylbenz[a]anthracene and benzo[a]pyrene in some of the repeated experiments, suggest unstable activity of enzymes involved in polycyclic aromatic hydrocarbons metabolism in these cell lines
TL;DR: Postpartum Wistar inbred rats (weaned on the 9th puerperal day) were injected intraductally in one mammary gland with 7,12-dimethylbenze (a) anthracene (DMBA) to selectively induce ductal carcinoma to be the cause of the development of atypical epithelial cells, inducingductal carcinomas.
Abstract: Postpartum Wistar inbred rats (weaned on the 9th puerperal day) were injected intraductally in one mammary gland with 7,12-dimethylbenze (a) anthracene (DMBA) to selectively induce ductal carcinoma. The incidence of ductal hyperplasia increased with time until it peaked at 7 weeks (12/13 animals) and then decreased. Ductal carcinoma first developed at 9 weeks in 3/12 (2 non-invasive and 1 invasive lesion) and the incidence increased with time until invasive ductal tumors were observed in 9/11 at 20 weeks. Tumors developed only in the DMBA-treated mammary glands and no systemic effects of the carcinogen were observed. Degeneration and detachment of epithelioglandular cells were seen here and there in the ducts and terminal ducts, and epithelioglandular cells proliferated in terminal duct until 2 weeks. Residual trace DMBA powder was detected in terminal ducts and the epithelioglandular layer until 7 weeks. This trace DMBA was considered to be the cause of the development of atypical epithelial cells, inducing ductal carcinomas.
TL;DR: The results of this study suggest that Sudan III-induced prevention of in vivo mutagenesis is due to the induction of both CYP 1A1 and detoxifying phase II enzymes, which may accelerate formation of active metabolic intermediates and detoxify these intermediates to inactive metabolites.
Abstract: Effect of the induction of drug metabolizing enzymes by Sudan III on the in vivo and in vitro genotoxicity elicited by 7,12-dimethyl-benz(a)anthracene (DMBA) was investigated. A significant suppression of DMBA-induced micronucleated reticulocytes was observed in C57BL/6 mice treated with Sudan III intraperitoneally for 3 or 5 days before injection of the DMBA. However, the preincubation of DMBA with hepatic microsomes from Sudan III-treated rats caused a marked increase in the in vitro mutagenicity in the Ames assay, paradoxically. Sudan III was found to induce CYP 1A1, 7-ethoxycoumarin O-deethylase activity as well as both UDP-glucuronyl transferase and glutathione S-transferase activities. The increase of mutagenicity of DMBA observed in the Ames assay using hepatic microsomes from Sudan III-treated rats was inhibited by the addition of uridine 5′-diphosphoglucuronic add or reduced glutathione with cytosol. Mutagenic metabolites of DMBA formed by CYP1A1 appeared to be effectively detoxified by these phase II enzymes.
The results of this study suggest that Sudan III-induced prevention of in vivo mutagenesis is due to the induction of both CYP 1A1 and detoxifying phase II enzymes. The induced CYP1A1 may accelerate formation of active metabolic intermediates, but phase II enzymes are also induced and detoxify these intermediates to inactive metabolites. This would reduce residence time of the carcinogen in the body and the time of exposure to active metabolites for target organs.
TL;DR: The administration of SPG enhanced the anti-tumor effect of CDDP, and an infiltrative increase in cytotoxic T-lymphocytes (CTL) was induced, although the development of helper T-cells and macrophages was immunohistochemically weak at the tumor site.
Abstract: Objective: Experimental chemotherapy was conducted to investigate the combined effect of Schizophyllan (SPG) and Cisplatin (CDDP).
Methods: Rats with 7,12-dimethylbenz(a)anthracene (DMBA)-induced ovarian adenocarcinoma received SPG and/or CDDP, were observed for the anti-tumor effect of the drugs and were subjected to immunohistochemical study.
Results: 1Tumor reduction was enhanced by the combined use of SPG and CDDP; 2The survival rate of rats given SPG alone was significantly higher than that of the control rats, and treatment with SPG combined with CDDP tended to improve the survival rate; 3Immunohistochemically, an infiltrative increase in cytotoxic T-lymphocytes (CTL) was induced, although the development of helper T-cells and macrophages was immunohistochemically weak at the tumor site.
Conclusion: The administration of SPG enhanced the anti-tumor effect of CDDP.
TL;DR: It is concluded that a cabbage diet during initiation has an inhibitory effect on hepatocarcinogenesis in toads.
Abstract: Hepatocellular carcinoma was induced in the toad, Bufo viridis, in 29 out of 100 cases by the administration of 0.5 mg of 7,12-dimethylbenz(a)anthracene (DMBA)/toad, 3 times/week for 12 weeks. In contrast, toads treated with DMBA and cabbage diet 1 or 2 ml (3 h prior to the carcinogen)/toad, every day for 12 weeks showed a lower incidence of liver tumors: 15 and 12 cases out of 100. However, cabbage diet (2 ml/toad, every day for 12 weeks) was ineffective when administered 3 h after the carcinogen (DMBA) in 27 out of 100 cases. Neither tumor growth nor neoplastic changes were observed in toads treated with olive oil alone or with cabbage diet. It is concluded that a cabbage diet during initiation has an inhibitory effect on hepatocarcinogenesis in toads.
TL;DR: An antioxidant role for selenium is suggested in experimental mammary tumor induced by dimethylbenz(a)anthracene and the increase in the levels of these enzymes was found to be predominantly significant in the liver.
Abstract: The biological impact of selenium on the levels of antioxidant enzymes in Wistar rats bearing mammary tumor induced by dimethylbenz(a)anthracene was investigated. Control rats and tumor-bearing rats were fed a normal diet or one containing 5mg sodium selenite/kg diet from the day of tumor induction. The reduced levels of ceruloplasmin, ascorbic acid, and α-tocopherol seen in the serum of tumor-bearing rats on the normal diet were found to be increased by the selenium treatment. The activities of superoxide dismutase and catalase in tumor-bearing rats were decreased significantly when compared with those of control rats, whereas selenium administration caused a considerable recovery of the activities of these enzymes in the rats with tumors. The increase in the levels of these enzymes was found to be predominantly significant in the liver. These observations clearly suggest an antioxidant role for selenium in experimental mammary tumor.
TL;DR: In this paper, the putative D-ring metabolites of 1,2,3,4-tetrahydro-7,12-dimethyl-benz[a]anthracene (1) and (8α,9α,10β,11α) were reported.
Abstract: Syntheses of (8α,9α,10α,11β)-trans-1,2,3,4,8,9,10,11-octahydro-7,12-dimethyl-8,9-epoxybenz[a]anthracene-10,11-diol (3) and (8α,9α,10β,11α)-trans-1,2,3,4,8,9,10,11-octahydro-7,12-dimethyl-8,9-epoxybenz[a]anthracene-10,11-diol (4), the putative D-ring metabolites of 1,2,3,4-tetrahydro-7,12-dimethyl-benz[a]anthracene (1), starting from 1,2,3,4-tetrahydro-10-methoxy-7,12-dimethylbenz[a]anthracene (11), are reported.
TL;DR: Sulfonation of resulting 6-hydroxymelatonin does not appear to have been assessed in a correct manner because the reaction was conducted without the biological sulfo-group donor or co-substrate, 3-phosphoadenosine-5'-phosphosulfate (PAPS), and it is unlikely that the sulfonation occurred to a significant extent.
Abstract: Praast and colleagues have reported that hepatic microsomal monooxygenase activity catalyzing the melatonin hydroxylation is strongly inducible by phenobarbital 1. The authors state that the resulting metabolite, 6-hydroxymelatonin undergoes phase II (conjugation) reactions such as glucuronidation and sulfation. In this study, urinary excretion of the sulfo-conjugated metabolite of 6-hydroxymelatonin was measured. Furthermore, the formation of 6-sulfooxymelatonin was examined by incubating melatonin or its 6-hydroxylated metabolite with rat liver postmitochondrial supernatant (S-9) enriched with the NADPH-regenerating system. Unfortunately, part of experimental procedures described in this paper are confusing and misleading. I have no objection to hydroxylation of melatonin by rat liver S-9 and NADPH. However, sulfonation of resulting 6-hydroxymelatonin does not appear to have been assessed in a correct manner because the reaction was conducted without the biological sulfo-group donor or co-substrate, 3'-phosphoadenosine-5'-phosphosulfate (PAPS). Since PAPS was not added to the incubation mixture, the sulfotransferase-mediated formation of 6sulfooxymelatonin from melatonin via 6-hydroxymelatonin or directly from the hydroxy substrate must have been solely dependent upon the presence of endogenous PAPS, and it is unlikely that the sulfonation occurred to a significant extent. Even though the radio-immuno assay employed in this study might be sensitive enough to detect the basal level of 6-sulfooxymelatonin, the amount of this polar metabolite is considered to have been underestimated because of limitations of the sulfogroup donor required for its formation by sulfotransferase activity. Addition of the NADPH-generating system was intended to facilitate the microsomal monooxygenase-mediated metabolism of melatonin to its 6-hydroxy derivative. However, the same cofactor system was also used for the determination of sulfonation of 6-hydroxymelatonin. This does not make any sense because the hydroxy derivative already bears a functional group that can be subjected to sulfo-conjugation. The presence of NADPH, on the contrary, would only complicate the reaction by producing secondary metabolite(s) through oxidation of 6-hydroxymelatonin, limiting its availability for the formation of 6-sulfooxymelatonin. Thus, due to omission of the sulfo-group donor and the inappropriate use of the NADPH-generating system, the accurate and precise quantitation of 6-sulfooxymelatonin from melatonin or 6-hydroxymelatonin could not be expected and the significance of in vitro formation of 6-sulfooxymelatonin addressed by the authors thus needs to be reconsidered. Finally, I would like to suggest that the term 'sulfonation' be used in place of 'sulfation' since sulfotransferases catalyze the transfer of the sulfo-group ( -SO;) , not the sulfate ( -S O ~) , from PAPS to the hydroxyl or amino groups of acceptor molecules 2. By analogy, the use of the prefix 'sulfooxy-' or 'sulfonoxy-' is a more appropriate nomenclature of designating sulfonated products, including the sulfo conjugate of 6-hydroxymelatonin, than the use of the unfamilar term 'sulfatoxy-' adopted by the authors.