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Biomedical subjects

H Mukhtar

Publications and source records attributed to H Mukhtar.

At least 289 records · Page 16Linked to original sources
PubMed1976

Glutathione-S-epoxide transferase activity during development and the effect of partial hepatectomy.

The specific activity of glutathione-S-epoxide transferase with styrene oxide and 3-methylcholanthrene-11, 12-oxide was determined in rat liver and lung during development from the fetal to the adult stage and after partial hepatectomy. Enzyme activity in fetal liver or lung at 18 days of gestation was about 20% of that observed in the adult; it rose rapidly to the adult value by 21 days of age. Hepatic enzyme activity was reduced to 50% of control values by 12 hr after partial hepatectomy; enzyme activity returned to control values by 48 hr. No diurnal variation in the activity of glutathione-S-epoxide transferase was observed in rat liver.

Animals↗
PubMed1973

Effect of high- and low-protein diets on the regulation of rat liver tyrosine aminotransferase and tryptophan oxygenase activities by L-tyrosine and L-tryptophan.

Induction of rat liver tyrosine aminotransferase by l-tyrosine and tryptophan oxygenase by l-tryptophan was studied in groups of rats fed on diets containing 18 or 5% protein. The basal activity of hepatic tyrosine aminotransferase of rats receiving 5% protein gradually increased with the age of the animals but that of rats receiving 18% protein did not. l-Tyrosine induced hepatic tyrosine aminotransferase in rats receiving 18% protein when tested at ages from 4 to 20 weeks. When induction by l-tyrosine was carried out in rats receiving the 5% protein diet, significant induction of tyrosine aminotransferase occurred only in 4- or 6-week-old rats. Induction by l-tryptophan of tryptophan oxygenase in liver or the basal activity of this enzyme in liver did not differ between the groups fed on 5 and 18% protein. On changing the diet from 0 to 18% protein, the above-mentioned effects on the induction of hepatic tyrosine aminotransferase were reversed.

Animals↗
PubMedDate not supplied

Epidermal enzyme-mediated mutagenicity of the skin carcinogen, 2-aminoanthracene.

Using four Salmonella typhimurium tester strains (TA1537, TA1538, TA98 and TA100) and the promutagen 2-aminoanthracene, an epidermal S9-mediated mutagenicity assay was developed. Using an activation mixture derived from whole skin of the rat, mutagenicity was observed in tester strain TA98 whereas an activation mixture derived from the dermis resulted in mutagenicity in tester strains TA1538, TA98 and TA100. Activation mixtures from both the epidermis and the liver produced a positive response in all of the tester strains studied. Activation mixtures from liver were shown to have the highest specific activity followed in decreasing order of potency by epidermis, dermis and whole skin. These results indicate that the skin, a target tissue directly exposed to environmental chemicals, is capable of converting 2-aminoanthracene to mutagenic moieties. Since the skin of the rat is known to be susceptible to tumor induction by 2-aminoanthracene our findings re-emphasize that membrane-bound enzymes can influence toxic responses including mutagenicity to xenobiotics in cutaneous tissue.

Animals↗
PubMedDate not supplied

Inhibition of the skin tumorigenicity of (+/-)-7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene by tannic acid, green tea polyphenols and quercetin in Sencar mice.

The effect of pretreatment of skin of Sencar mice with topically applied tannic acid, quercetin and green tea polyphenols (GTP) on the skin tumor initiating activity of (+/-)-7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE-2) has been evaluated. The animals were pretreated with the plant phenols (tannic acid and quercetin (3000 nmol) or GTP 24 mg/mouse) for 7 days after which they received a single topical application of 200 nmol of BPDE-2 as the initiating agent. Beginning 7 days following initiation animals received twice weekly applications of 3.24 nmol of 12-O-tetradecanoyl phorbol-13-acetate (TPA). Tannic acid and GTP afforded significant protection against skin tumor induction. These inhibitory effects were verified both by prolongation of the latency period and subsequent development of tumors. Quercetin, on the other hand, afforded only moderate protection. Each phenolic compound was found to be highly effective in accelerating the disappearance of BPDE-2 from aqueous medium. Our results suggest that tannic acid and GTP have substantial potential for protecting against the skin tumorigenic response to BPDE-2 and the mechanism of inhibition may involve inactivation of the reactive carcinogenic moiety.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMedDate not supplied

Azole antifungals.

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Antifungal Agents↗
PubMedDate not supplied

Photocarcinogenesis.

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Animals↗
PubMedDate not supplied

Perspectives of photodynamic therapy for skin diseases.

Photodynamic therapy (PDT) is largely an experimental modality for the treatment of neoplastic and selected nonneoplastic diseases. This therapeutic procedure, through a cascade of events, leads to cell killing. In the past few years, dermatology has taken advantage of PDT for the treatment of skin cancer and other skin diseases. The skin has considerable attributes over many other organs for the application of PDT. These include the accessibility to all three PDT essential requirements; the drug (photosensitizing agent), visible light and oxygen. The major benefit of experimental PDT in dermatology is the ability to assess the clinical response visually and the relative ease in obtaining biopsies for precise biochemical and histological analysis. Currently, PDT has received approval worldwide for the ablation of various tumor types. In the United States, the Food and Drug Administration has approved PDT for the treatment of advanced esophageal cancer and selected patients with lung cancer. Clinical trials, employing several types of photosensitizers for PDT, are ongoing for a variety of dermatological lesions. This review summarizes current knowledge of PDT in dermatology and highlights future perspectives of this modality for effective management of skin diseases.

Humans↗
PubMedDate not supplied

Biomelanin antioxidants in cosmetics: assessment based on inhibition of lipid peroxidation.

Acute adverse effects of ultraviolet (UV) radiation in humans include sunburn, photosensitivity reactions and immunological suppression. Chronic exposure to UV light, particularly the UVB (290-320 nm) component of the UV radiation, and certain environmental chemicals increase the risk of nonmelanoma skin cancer and play a major role in cutaneous aging. The lipid peroxidation (LPO) of biomembranes, mediated by reactive oxygen species and free radicals, is one of the major causes of cellular damage induced by UV radiation and toxins. Antioxidants, such as vitamin E, vitamin C and melanins, are reactive oxygen and radical scavengers, thereby minimizing the light- and toxin-induced tissue destruction. We examined the influence of 8 biotechnically produced polyphenolic melanins on the LPO of microsomal membranes in comparison with alpha-tocopherol, ascorbate and synthetic melanin. All biomelanins showed better inhibition of peroxidative damage than synthetic melanin. Three of the 8 tested drugs inhibited the LPO at least as effectively as vitamin C and vitamin E. The combination of the most effective biomelanin with both vitamin C and vitamin E resulted in greater LPO inhibition than caused by each agent alone. Our data show that biomelanins are potent inhibitors of the peroxidative destruction of biomembranes, indicating that these compounds may be useful antioxidative agents in cosmetic preparations.

Animals↗