Search PubMed⌕ Search

Biomedical subjects

H Mukhtar

Publications and source records attributed to H Mukhtar.

At least 109 records · Page 6Linked to original sources
PubMed1995

Inhibition of ras p21 membrane localization and modulation of protein kinase C isozyme expression during regression of chemical carcinogen-induced murine skin tumors by lovastatin.

We investigated the ras p21 membrane localization and the expression and activation of protein kinase C (PKC) isozymes in activated ras oncogene-containing tumors and assessed whether these events were related to tumor growth. We used 7,12-dimethylbenz[a]anthracene-initiated and 12-O-tetradecanoylphorbol-13-acetate-promoted SENCAR mouse skin tumors, which were shown to contain Ha-ras oncogene activated by point mutation at codon 61, as an in vivo model for these studies. Compared with levels in epidermis, highly elevated levels of membrane-bound Ha-ras p21 were observed in growing tumors, which also showed strong expression and membrane translocation of PKC zeta and beta II and weak expression of PCK alpha. However, when ras p21 membrane localization was blocked in vivo in growing tumors by lovastatin, opposite results were evident. Compared with saline-treated animals, in which tumor growth continued, lovastatin-treated animals had significantly inhibited tumor growth, which led to tumor regression with concomitant inhibition of Ha-ras p21 membrane localization. These regressing tumors from lovastatin-treated animals also showed a decrease in the expression and membrane translocation of PKC zeta and beta II but increased expression of PKC alpha. Taken together, our results indicate that ras p21 membrane localization and the expression and activation of PKC zeta, beta II, and alpha may be the critical events in the regulation of the growth of tumors that contain activated ras oncogenes.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1995

A rapid and convenient filter-binding assay for ras p21 processing enzyme farnesyltransferase.

Because it is the target for the development of anti-cancer agents, the mammalian cytosolic enzyme farnesyltransferase (FTase) has received significant attention in recent years. FTase catalyzes the transfer of a farnesyl group from farnesylpyrophosphate (FPP) to cysteine 185/186 at the carboxyl terminal end of ras proteins (ras p21), a reaction essential for the localization of ras p21 to the plasma membrane for their cellular functions including cell transformation in case of oncogenic ras p21. Here, we report the development of a rapid and convenient assay procedure for FTase using phosphocellulose paper which has a binding affinity for proteins. The FTase is assayed as the transfer of [3H]farnesyl group from [3H]FPP to the ras p21 at pH 7.4 and 37 degrees C in the presence of rat brain cytosol followed by the binding of radioactive farnesylated ras p21 to the phosphocellulose paper. The radioactivity associated with ras p21 bound to the phosphocellulose paper was determined by scintillation counting after soaking the paper in trichloroacetic acid and washing with distilled water. Utilizing [3H]FPP and recombinant Ha-ras p21 as substrates in the reaction, the FTase followed Michaelis-Menten kinetics with Km values of 1.0 and 7.69 microM for respectively [3H]FPP and recombinant Ha-ras p21. The method reported here has the advantages over the other published assay procedures of being rapid, convenient and economical, and can be successfully used for the basic assaying of FTase in different organs and distinct species and for the screening of novel inhibitors of FTase.

Alkyl and Aryl Transferases↗
PubMed1995

Differential response of normal and HPV immortalized ectocervical epithelial cells to B[a]P.

Cigarette smoking has been established as a risk factor for the development of cervical cancer. Polycyclic aromatic hydrocarbons such as benzo[a]pyrene (B[a]P), which are present in cigarette smoke, might account for this increased risk. The effects of B[a]P on cell growth, aryl hydrocarbon hydroxylase, DNA adducts and p53 levels was measured in cervical cells. Since 90% of cervical preneoplastic lesions are positive for the human papillomavirus (HPV) we compared the effects of these chemicals in normal ectocervical epithelial cells (ECE) and human papillomavirus 16 (HPV16) immortalized ectocervical epithelial cells (ECE16-1). Exposure of normal ECE and HPV immortalized ECE16-1 cells to B[a]P inhibited cell proliferation. Inhibition occurred at 20-fold lower concentrations in the normal ECE cells compared to ECE16-1 cells. The proliferation of cervical cells which express mutated p53 was unaffected by B[a]P. Neither cervical stromal cells nor endometrial stromal cells were affected by these compounds. The effects of B[a]P on normal ECE cell proliferation correlated with increased terminal differentiation as measured by increased envelope formation. In contrast, B[a]P exposure did not induce envelope formation in immortalized ECE16-1 cells or in cervical tumor cells. Pretreatment of both ECE and ECE16-1 cells with 2,3,7,8-tetrachlorodibenzo-p-dioxin, which induces P450 expression and activity, did not alter B[a]P metabolism in either normal or immortalized cells. Furthermore, equivalent levels of DNA adducts were formed by B[a]P in ECE and ECE16-1 cells. Neither the extent of adduct formation nor the rate of their removal differed in normal and immortalized cervical cells. Therefore, the diminished growth inhibition of the ECE16-1 cells as compared to normal ECE cells by B[a]P is not due to changes in cytochrome P450 of the 1A family metabolism or DNA adduct number. Furthermore, analysis of the p53 levels in both normal and ECE16-1 cells revealed that p53 levels are higher in normal versus immortalized ectocervical cells, and p53 is induced in both cell types following B[a]P treatment. Thus reduced p53 levels in ECE16-1 cells may contribute to a lack of growth suppression following B[a]P treatment. These results demonstrate that HPV16 immortalization diminishes ectocervical epithelial cell responsiveness to toxicant damage (i.e. decreased cell proliferation and increased terminal differentiation). As a result, ECE16-1 cells that sustain genotoxic damage which leads to DNA adduct formation continue to proliferate and may be at increased risk for mutations and further progression towards a fully transformed phenotype.

Benzo(a)pyrene↗
PubMed1995

Inhibition of 12-O-tetradecanoylphorbol-13-acetate and other skin tumor-promoter-caused induction of epidermal interleukin-1 alpha mRNA and protein expression in SENCAR mice by green tea polyphenols.

Recent studies have shown that topical application of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) to murine skin results in increased expression of the highly inflammatory cytokine interleukin (IL)-1 alpha in the epidermis. This has led to the suggestion that IL-1 alpha directly or indirectly mediates the inflammatory and hyperplastic responses elicited by TPA and possibly by other skin tumor promoters. In the current study, we investigated the effect of skin application of a polyphenolic fraction isolated from green tea (GTP) to SENCAR mice on skin tumor-promoter-caused induction of cutaneous edema and hyperplasia, and IL-1 alpha mRNA expression. Pretreatment of the skin with GTP 30 min before that of anthralin, benzoyl peroxide, mezerein, and TPA resulted in a significant (p < 0.05) inhibition of cutaneous edema and epidermal hyperplasia caused by each of these tumor promoters. Northern blot analysis indicated that topical application of TPA, anthralin, mezerein, or benzoyl peroxide to SENCAR mice resulted in an increased expression of epidermal IL-1 alpha mRNA. Pretreatment of the skin with GTP or individual epicatechin derivatives (ECDs) present therein, 30 min before that of TPA, resulted in a significant inhibition of enhanced expression of epidermal IL-1 alpha mRNA caused by skin application of TPA. These inhibitory effects were found to be dependent on the dose of GTP. Among four epicatechin derivatives present in GTP, (-)-epicatechin-3-gallate and (-)-epigallocatechin-3-gallate were more effective than (-)-epigallocatechin and (-)-epicatechin in affording this inhibition. Preapplication of GTP was also found to afford inhibition against anthralin-, benzoyl peroxide-, and mezerein-caused increased expression of epidermal IL-1 alpha mRNA and protein. Our study suggests that the inhibition of tumor-promoter-induced IL-1 alpha mRNA and protein expression in mouse epidermis by green tea in combination with other inhibitory effects may be responsible for the anti-tumor-promoting and anti-inflammatory effects of GTP.

Animals↗
PubMed1995

Protection against ultraviolet-B radiation-induced local and systemic suppression of contact hypersensitivity and edema responses in C3H/HeN mice by green tea polyphenols.

Exposure of skin to UV radiation can cause diverse biological effects, including induction of inflammation, alteration in cutaneous immune cells and impairment of contact hypersensitivity (CHS) responses. Our laboratory has demonstrated that oral feeding as well as topical application of a polyphenolic fraction isolated from green tea (GTP) affords protection against the carcinogenic effects of UVB (280-320 nm) radiation. In this study, we investigated whether GTP could protect against UVB-induced immunosuppression and cutaneous inflammatory responses in C3H mice. Immunosuppression was assessed by contact sensitization with 2,4-dinitrofluorobenzene applied to UVB-irradiated skin (local suppression) or to a distant site (systemic suppression), while double skin-fold swelling was used as the measure of UVB-induced inflammation. Topical application of GTP (1-6 mg/animal), 30 min prior to or 30 min after exposure to a single dose of UVB (2 kJ/m2) resulted in significant protection against local (25-90%) and systemic suppression (23-95%) of CHS and inflammation in mouse dorsal skin (70-80%). These protective effects were dependent on the dose of GTP employed; increasing the dose (1-6 mg/animal) resulted in an increased protective effect (25-93%). The protective effects were also dependent on the dose of UVB (2-32 kJ/m2). Among the four major epicatechin derivatives present in GTP, (-)-epigallocatechin-3-gallate, the major constituent in GTP, was found to be the most effective in affording protection against UVB-caused CHS and inflammatory responses. Our study suggests that green tea, specifically polyphenols present therein, may be useful against inflammatory dermatoses and immunosuppression caused by solar radiation.

Animals↗
PubMed1994

Inhibition of spontaneous and photo-enhanced lipid peroxidation in mouse epidermal microsomes by epicatechin derivatives from green tea.

In recent years green tea has been shown to afford protection against chemical- and photo-carcinogenesis in several animal tumor bioassay systems. It has been suggested that the wide range of anticarcinogenic properties of green tea may be due to the antioxidant effect of epicatechins present therein. In this study, we assessed whether these epicatechin derivatives (ECDs)--namely (-)-epigallocatechin (EGC), (-)-epicatechin gallate (ECG), (-)-epigallocatechin-3-gallate (EGCG) and (-)-epicatechin (EC) inhibit spontaneous and photo-enhanced lipid peroxidation (LPO) in mouse epidermal microsomes. Our data indicate that significant inhibition (significance levels for P, < 0.05 to < 0.0001) was evident by EGCG, EGC and ECG in Fe3+/ADP supported LPO. Interestingly each of these epicatechin derivatives was also effective in inhibiting photo-enhanced LPO generated by incubating epidermal microsomes in the presence of silicon phthalocyanine and 650 nm irradiation. However, at equimolar basis, EGCG, which is also the major constituent in GTP, showed maximum inhibitory effects compared to other ECDs. Taken together, our results provide the direct evidence for the antioxidant property of ECDs, and suggest that such an effect may contribute towards anticarcinogenic (specifically anti-skin tumor) promoting effects of green tea.

Animals↗
PubMed1994

Evidence for multiple inducible cytochrome P450 isozymes in SENCAR mouse skin by pyridine.

Pyridine, an amphipathic solvent, is widely used in industry and is also a constituent of tobacco and its smoke. Since, in addition to inhalation and ingestion, pyridine is also readily absorbed through skin, we assessed the effect of skin application of pyridine on monooxygenase activities and cytochrome P450 (CYP) isozymes and CYP mRNA levels in the skin of SENCAR mice. Compared to controls, a single topical application of pyridine (30 or 50 mg/100 g body weight) resulted in induction of cutaneous 7-ethoxyresorufin O-deethylase, 7-pentoxyresorufin O-depentylase, and erythromycin N-demethylase activities. Pyridine treatment also resulted in an increase in reactivity with monoclonal antibodies directed against CYP 1A1, 2B1 and 3A. In Northern blot analysis, treatment of pyridine also showed a significant increase in mRNA for Cyp1a-1 in the skin. These data indicate that murine skin contains multiple inducible CYP isozymes, and that pyridine results in the induction of at least three families of CYP in murine skin.

Animals↗
PubMed1994

Studies on the activity of Kluyveromyces lactis S-adenosylmethionine: delta 24-sterol methyltransferase in presence of polyenic antifungal agents.

The S-adenosylmethionine: delta 24-sterol methyltransferase (24 SMT) primarily considered as a mitochondrial enzyme, was recently mainly detected in lipid particles of yeasts. It catalyses the methylation of zymosterol which is an essential reaction for the synthesis of ergosterol. We have investigated in cellular extracts of two Kluyveromyces lactis strains the action of polyenic antifungal agents on the activity of this enzyme. Low concentrations of amphotericin B, candicidin and pimaricin strongly stimulate this activity, while high concentrations inhibit it or have no effect. Whatever the doses used, nystatin and filipin had no significant influence on this activity. According to the molar ratio amphotericin B/total sterols of the enzyme preparation, the interference of amphotericin B on the 24 SMT activity may result of two mechanisms.

Amphotericin B↗
PubMed1994

Inhibitory effect of silymarin, an anti-hepatotoxic flavonoid, on 12-O-tetradecanoylphorbol-13-acetate-induced epidermal ornithine decarboxylase activity and mRNA in SENCAR mice.

In recent years, considerable emphasis has been placed on identifying new cancer chemopreventive agents which could be useful for human populations. Silymarin, an anti-oxidant flavonoid isolated from artichoke, has been shown to possess significant activity against hepatotoxicity and other pharmacological and physiological disorders. Since many antioxidants inhibit tumor promotion, and because ornithine decarboxylase (ODC) is a well known biochemical marker of tumor promotion, we assessed the effect of skin application of silymarin on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced epidermal ODC activity and ODC mRNA levels in SENCAR mice. Application of silymarin at doses of 0.5-18 mg (1-37 mumol)/mouse prior to that of TPA (2.5 micrograms) treatment resulted in significant inhibition of TPA-induced epidermal ODC activity in a dose- and time-dependent manner. Northern blot analysis revealed that topical application of silymarin at the dose of 2 mg/mouse resulted in almost complete inhibition of TPA-induced epidermal ODC mRNA. In other studies, silymarin also showed significant inhibition of epidermal ODC activity induced by several other tumor promoters, including free radical-generating compounds. Our data suggest that silymarin could be a useful anti-tumor promoting agent capable of ameliorating the tumor promoting effects of a wide range of tumor promoters.

Animals↗
PubMed1994

Green tea and skin--anticarcinogenic effects.

Because of its special aroma, green tea is a popular beverage consumed by some human populations worldwide. In recent years, many laboratory studies have shown that in a variety of animal tumor bioassay systems the administration of green tea, specifically the polyphenolic fraction isolated from green tea leaves (green tea polyphenols), affords protection against cancer induction. In mouse skin tumor bioassay systems, topical application of green tea polyphenols to skin has been shown to result in protection against a) 3-methylcholanthrene-induced skin tumorigenicity, b) 7,12-dimethylbenz(a)anthracene (DMBA)-induced skin tumor initiation, c) 12-O-tetradecanoylphorbol-13-acetate and other tumor promoters caused tumor promotion in DMBA-initiated skin, and d) benzoyl peroxide- and 4-nitroquinoline N-oxide caused enhanced malignant progression of nonmalignant lesions. Green tea extract has also been shown to cause partial regression of established skin papillomas in mouse. Similarly, chronic oral feeding of green tea polyphenols or water extract of green tea has also been shown to result in the protection against both chemical carcinogen- and ultraviolet B radiation-induced skin tumorigenicity. Collectively these data suggest that green tea possesses significant chemopreventive effect against each stage of carcinogenesis, and that it may be useful against inflammatory responses associated with the exposure of skin to chemical tumor promoters as well as to solar radiation. Available data regarding the mechanism by which green tea affords these diversified effects is discussed.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1994

Ras p21 farnesylation in ultraviolet B radiation-induced tumors in the skin of SKH-1 hairless mice.

Cutaneous exposure to solar ultraviolet B (UVB) radiation is well recognized as the major cause of skin cancer in humans; however, the precise molecular mechanisms whereby UVB mediates carcinogenesis remains unclear. The involvement of activated ras oncogenes has been demonstrated extensively in both animal and human skin cancers. Activated ras oncogenes encode mutated ras p21 that exist in the guanosine triphosphate-bound active state and, following localization to the inner side of the plasma membrane, cause cellular transformation. This membrane association requires three post-translational modifications occurring at the C-terminus of the ras p21. The farnesylation of p21 by a cytosolic enzyme known as farnesyltransferase (FTase) is the critical step that triggers biologic functions of the ras p21. In this study, FTase activity was found to be substantially higher (approximately threefold) in UVB radiation-induced tumors in SKH-1 hairless mice compared to epidermis from controls. Western blot analysis showed significantly higher levels of Ha-ras p21 in both cytosolic and membrane fractions prepared from tumors compared to epidermis. Pan ras antibody against mutated p21 at codon 12 showed very strong reactivity for ras val-12p21 in tumors but not in normal epidermis, suggesting a gly to val substitution at 12th position in ras p21 in UVB-induced tumors. Our data indicate that enhanced FTase activity and the processing of overexpressed p21 in UVB-induced tumors are correlated, and predict the role of point mutation at the 12th codon of the ras oncogene during photocarcinogenesis in mice.

Alkyl and Aryl Transferases↗
PubMed1994

Multiple cytochrome P450 isozymes in murine skin: induction of P450 1A, 2B, 2E, and 3A by dexamethasone.

Cytochrome P450s (P450s) are a supergene family of enzymes responsible for the metabolism of a wide range of endogenous and foreign compounds. P450 isozymes possess overlapping substrate specificity. Systemic administration of dexamethasone, a widely used topical agent in dermatologic practice, to animals is known to result in the induction of multiple P450 isozymes in liver. In this study the effect of topical application of dexamethasone to mice on P450-dependent monooxygenase activities, expression of P450 isozymes, and P450 mRNA levels in skin was assessed. The treatment of mice with dexamethasone resulted in significant induction of 7-ethoxyresorufin O-deethylase (2.3 times), 7-pentoxyresorufin O-depentylase (19.2 times), para-nitrophenol hydroxylase (7.5 times), and erythromycin N-demethylase (2.2 times) activities; the monooxygenases catalyzed preferentially by P450 isozymes 1A1, 2B1, 2E1, and 3A, respectively. Immunoblot analysis of cutaneous microsomes, employing antibodies directed against purified P450s 1A1/2, 2B1/2, 2E1, and 3A, showed that dexamethasone treatment results in an increased immunoreactivity (1.8-13.9 times). In immunohistochemical staining of skin with antibody against P4502B1/2, topical application of dexamethasone resulted in an increased reactivity towards microsomal protein in the suprabasal layer of the epidermis and with the cells of the hair follicles. Whereas constitutive expression of mRNAs for CYP1A1 and CYP2E1 was evident in murine skin, any change in the levels of these mRNAs following treatment with dexamethasone was not apparent. The results of our study indicate that the application of dexamethasone to murine skin results in the induction of several families of P450 isozymes, suggesting that murine skin contains multiple inducible P450 isozymes capable of participating in the metabolism of a wide range of xenobiotics and endogenous compounds.

Administration, Topical↗
PubMed1993

Phospholipase activation triggers apoptosis in photosensitized mouse lymphoma cells.

Photodynamic therapy (PDT), an experimental cancer treatment employing a photosensitizer and visible light, is a highly efficient inducer of apoptosis (or programmed cell death) in mouse L5178Y lymphoma cells, resulting in extensive DNA fragmentation within 1-2 h. The major targets for PDT are in cellular membranes, and we now find that PDT sensitized by aluminum phthalocyanine causes the rapid (< 1 min) activation of phospholipase C and the breakdown of membrane phosphoinositides, as well as a similarly rapid release of Ca2+ from intracellular pools. A phospholipase C inhibitor, U73122, blocks the rapid transient increases in both inositol-1,4,5-trisphosphate and intracellular Ca2+ levels as well as the subsequent fragmentation of nuclear DNA, whereas the analogue U73343 is much less effective against all of the aforementioned responses. In addition, p-bromphenacyl bromide, an inhibitor of phospholipase A2, blocks DNA fragmentation, and PDT stimulates the release of arachidonic acid, probably by phospholipase A2-dependent breakdown of membrane phospholipids. Thus, photodynamic damage to cell membranes can mimic natural stimuli of phospholipases and initiate apoptosis in L5178Y cells.

Animals↗
PubMed1993

Protection against malignant conversion of chemically induced benign skin papillomas to squamous cell carcinomas in SENCAR mice by a polyphenolic fraction isolated from green tea.

Progression of benign tumors to malignant cancer is critical since cancerous lesions are capable of metastatic spread and eventually causing death. Inhibitors of the conversion process, therefore, would likely be useful as cancer chemopreventive agents. In this study, we assessed the protective effect of topical application of a polyphenolic fraction isolated from green tea (GTP) against spontaneous as well as benzoyl peroxide (BPO)- and 4-nitroquinoline-N-oxide (4-NQO)-enhanced malignant conversion of chemically induced skin papillomas in SENCAR mice. Papillomas were induced in SENCAR mice by topical application of 7,12-dimethylbenz(a)anthracene as a tumor-initiating agent followed by twice a week application of 12-O-tetradecanoylphorbol-13-acetate as a tumor-promoting agent. Beginning at the 20th week, when papilloma yield was stabilized, enhanced malignant conversion was achieved by twice weekly topical application of either BPO or 4-NQO, whereas spontaneous malignant conversion was associated with topical application of acetone. In these protocols, preapplication of GTP (6 mg/animal) 30 min prior to skin application of acetone, BPO, or 4-NQO resulted in 14, 31, and 29% protection, respectively, in terms of percentage of mice with carcinomas, and 20, 35, and 43% protection in terms of number of carcinomas/mouse. In these experiments, a BPO- and 4-NQO-enhanced rate of malignant conversion was also found to be decreased significantly by the skin application of GTP; however, such effects of GTP were less profound in the cases of spontaneous malignant conversion. The results of this study suggest that, in addition to its chemopreventive effects against tumor initiation and promotion stages of multistage carcinogenesis, green tea also possesses significant protective effects against tumor progression, specifically tumor progression induced by BPO and 4-NQO.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1993

Protective effects of green tea polyphenols administered by oral intubation against chemical carcinogen-induced forestomach and pulmonary neoplasia in A/J mice.

Our studies and others have shown the cancer chemopreventive effects of chronic administration of green tea in several animal tumor models. In this study, the administration of a polyphenolic fraction isolated from green tea (GTP) by oral intubation at a dose of 5 mg in 0.2 ml water 30 min prior to challenge with carcinogen, afforded significant protection against both diethylnitrosamine (DEN)- and benzo(a)pyrene (BP)-induced forestomach and lung tumorigenesis in A/J mice. The protective effects were evident by a decrease in numbers of tumors/mouse in GTP-fed groups compared to non GTP-fed controls. In the forestomach tumorigenesis protocol, GTP afforded 71 and 66% protection against, respectively DEN- and BP-induced tumor multiplicity. In the case of lung tumorigenesis protocol, however, the protective effects of GTP were 41 and 39%, respectively. Histological examination of forestomach tumors showed significantly lesser number of squamous cell carcinoma formation in GTP-fed groups of mice compared to carcinogen alone-treated controls. When pulmonary tumors were examined histologically, no adenocarcinomas were observed in GTP-fed groups compared to 15% mice with adenocarcinomas in DEN and BP alone-treated controls. The results of this study suggest that limited doses of GTP administration by gavage 30 min prior to carcinogen challenge may afford protection against carcinogen-induced tumorigenesis in internal body organs.

Administration, Oral↗
PubMed1993

Glutathione S-transferases of human skin: qualitative and quantitative differences in men and women.

Glutathione S-transferase (GST) isozymes of male and female leg skin have been characterized. GST activities and protein have been quantified in a number of male and female skin samples and the results indicate that as compared to the male skin, female skin contains a higher amount of GST activity as well as protein. Both male and female leg skin contain three GST isozymes with pI values 9.9, 9.1 and 4.8. In accordance with previous findings the major isozyme, pI 4.8 belongs to the pi-class, whereas the two minor forms pI 9.1 and 9.9 belong to the alpha-class. Each of the three isozymes is more abundant in female skin. Surprisingly, the specific activities and Kcat values of the female skin GSTs, particularly of the pi-class isozyme were found to be significantly higher as compared to those of male skin isozyme. Studies into the kinetics of inhibition by hematin also indicated differences in male and female skin GSTs. Whereas we confirm the presence of an alpha-class GST, pI 9.9, in human skin with an apparently higher subunit M(r) value as compared to other human alpha-class GSTs, contrary to the previous report (Del Boccio et al. (1987) Biochem. J. 244, 21-25), the results of the present studies show that the N-terminus of this alpha-class GST is blocked.

Amputation, Surgical↗