OBJECTIVES

Carica papaya has been widely used commercially for skin care due to its therapeutic benefits. The potential of its flower to promote hair growth has been traditionally recognized in other countries but not in the Philippines. In this study, we explored the effect of various extracts of C. papaya flower in the biological activities associated with hair loss, including 5α-reductase inhibition and antioxidation, as well as identified the putative compounds present in the most potent extract.

The flowers of C. papaya were macerated separately with ethanol, ethyl acetate, and hexane to obtain their corresponding crude extracts. These extracts were subjected to antioxidant tests via 2,2′-diphenyl-1-picrylhydrazyl (DPPH), and ferric-reducing antioxidant power (FRAP) assays. The total phenolic and flavonoid contents (TPC and TFC) of the crude extracts were determined, as well as the ability of the extracts to inhibit 5α-reductase. The compounds present in the most potent extract were determined using ultraperformance liquid chromatography quadrupole time of flight mass spectrometer (UPLC/MS-QToF).

Ethyl acetate extract displayed significantly higher DPPH activity (0.001755 ± 0.00092 ascorbic acid equivalent antioxidant capacity) and 5α-reductase inhibitory activity (115.18 ± 11.61 mg dutasteride/g) compared to ethanol (DPPH: p=0.0121; 5α-reductase: p=0.0016) and hexane (DPPH: p=0.0038; 5α-reductase: p < 0.0001) extracts. Similarly, ethyl acetate extract gave the highest FRAP (0.4842 ± 0.0936 mg ascorbic acid/g) activity, TFC (0.0403 mg quercetin/g), and TPC (0.0463 mg gallic acid/g) among the extracts. Forty-nine compounds were annotated in the ethyl acetate extract, with seven (7) putatively identified as fatty acids (9-hydroxy-10,12-pentadecadienoic acid, 9,12,15-octadecatrienoic acid), hydroxyflavone (5-methylkaempferol), alkaloid (allomatrine), dipeptide derivative (aurantiamide acetate), bufotalinin, and 6β-acetoxy-5-epilimonin based on the Traditional Chinese Medicine Library.

These results suggest that local C. papaya flowers can be a source of hair growth-promoting agents via their antioxidant and 5α-reductase inhibitory potential.

BACKGROUND: It has recently been demonstrated that human hair also contains lipids. On the hair surface, the lipid layer is attached to the outer surface of hair covalently bonded to hair proteins. However, there have been no reports on lipid distribution in human hair follicles yet. OBJECTIVE: The purpose of this study was to demonstrate the lipids of the hair follicle and its distribution and also to examine the lipid composition of the hair follicle. MATERIAL AND METHODS: Follicles were obtained from the occipital region of the scalp which were not under the influence of anagen hormone. The specimens were stained using typical methods of oil red O, Holzinger's copper-rubeanic acid modification, perchloric acid-naphthoquinone reaction. RESULTS: Oil red O staining that could be used to stain all lipids was well detected in the area, Henle's layer of inner root sheath (IRS), IRS cuticle, and hair cuticle, which were keratinzed earlier in the hair follicle. The hair cuticle and the IRS were stained dark green on Holzinger's copper-rubeanic acid modification that could be used to stain free fatty acids. The IRS was stained gray-blue on perchloric acid-naphthoquinone reaction method that could be used to stain cholesterol and its esters. CONCLUSION: The present results demonstrate that the lipids of the hair follicle are located on the hair cuticle and the keratinized area of the IRS. They can act as a barrier of the hair follicle.
Cholesterol ; Esters ; Fatty Acids, Nonesterified ; Hair Follicle* ; Hair* ; Humans* ; Scalp

Stratum corneum lipids, which are enriched in sphingolipids, free fatty acids, and cholesterol, are required for epidermal barrier function. When the epidermal permeability barrier is perturbed, the transepidermal water loss returns to normal by 24-48 hours in parallel with the reappearance of stratum corneum lipids, derived from secreted lamellar bodis and accelerated lipid synthesis. Recent evidence shows that topical application of individual lipids interferes with barrier recovery while complete mixtures of cholesterol, fatty acids, and ceramides facilitate recovery after barrier disrupton. Metabolic imbalances and perturbed barrier function can be either the cause or the consequences of the pathobiology of scaling disease. Many skin diseases relating cornification and dryness are indeed related to abnormality of one or several combinations of lipids. Recently the cytokines which have changed during barrier recovery seem to be important in understanding of epidermal lipid homeostasis as well as barrier recovery.
Ceramides ; Cholesterol ; Cytokines ; Fatty Acids ; Fatty Acids, Nonesterified ; Homeostasis* ; Permeability ; Skin Diseases ; Sphingolipids ; Water

The present study was designed to assess the roles of PLA2 activation and arachidonic acid (AA) metabolites in hypoxia-induced renal cell injury. Hypoxia increased LDH release in a dose-dependent manner in rabbit renal cortical slices, and this increase was significant after 20-min hypoxia. The hypoxia-induced LDH release was prevented by amino acids, glycine and alanine, and extracellular acidosis (pH 6.0). Buffering intracellular Ca2+ by a chelator, but not omission of Ca2+ in the medium produced a significant reduction in hypoxia-induced LDH release. The effect of hypoxia was blocked by PLA2 inhibitors, mepacrine, butacaine, and dibucaine. A similar effect was observed by a 85-kD cPLA2 inhibitor AACOCF3. AA increased hypoxia-induced LDH release, and albumin, a fatty acid absorbent, prevented the LDH release, suggesting that free fatty acids are involved in hypoxia-induced cell injury. These results suggest that PLA2 activation and its metabolic products play important roles in pathogenesis of hypoxia-induced cell injury in rabbit renal cortical slices.
Acidosis ; Alanine ; Amino Acids ; Anoxia ; Arachidonic Acid ; Dibucaine ; Fatty Acids, Nonesterified ; Glycine ; Phospholipases A2* ; Phospholipases* ; Quinacrine

BACKGROUND: Malassezia species (spp.) are cutaneous opportunistic pathogens and associated with various dermatological diseases including seborrheic dermatitis, dandruff and atopic dermatitis. Almost all Malassezia spp. are obligatorily lipid-dependent, which might be caused by lack of the myristic acid synthesis. Recent genome analysis of M. restricta and M. globosa suggested that the absence of a gene encoding fatty acid synthesis might be compensated by abundant genes encoding hydrolases, which produce fatty acids, and that lipases and phospholipases may play a role in virulence of the fungus. OBJECTIVE: The current study aimed to investigate the contribution of lipases and phospholipases in virulence of the M. restricta as being the most frequently isolated Malassezia spp. from the human skin. METHODS: Swap samples of two different body sites of at least 18 patients with seborrheic dermatitis were obtained and in vivo expression of lipases and phospholipases of M. restricta was analyzed by the gene specific two-step nested RT-PCR. RESULTS: The results of the current study suggest that majority of the patients display expression of lipase RES_0242. CONCLUSION: These data imply a possible role of lipase in the host environment to produce free fatty acids for the fungus.
Dermatitis, Atopic ; Dermatitis, Seborrheic ; Fatty Acids ; Fatty Acids, Nonesterified ; Fungi ; Genes, vif ; Genome ; Humans ; Hydrolases ; Lipase ; Malassezia ; Myristic Acid ; Phospholipases

BACKGROUND: Malassezia species (spp.) are cutaneous opportunistic pathogens and associated with various dermatological diseases including seborrheic dermatitis, dandruff and atopic dermatitis. Almost all Malassezia spp. are obligatorily lipid-dependent, which might be caused by lack of the myristic acid synthesis. Recent genome analysis of M. restricta and M. globosa suggested that the absence of a gene encoding fatty acid synthesis might be compensated by abundant genes encoding hydrolases, which produce fatty acids, and that lipases and phospholipases may play a role in virulence of the fungus. OBJECTIVE: The current study aimed to investigate the contribution of lipases and phospholipases in virulence of the M. restricta as being the most frequently isolated Malassezia spp. from the human skin. METHODS: Swap samples of two different body sites of at least 18 patients with seborrheic dermatitis were obtained and in vivo expression of lipases and phospholipases of M. restricta was analyzed by the gene specific two-step nested RT-PCR. RESULTS: The results of the current study suggest that majority of the patients display expression of lipase RES_0242. CONCLUSION: These data imply a possible role of lipase in the host environment to produce free fatty acids for the fungus.
Dermatitis, Atopic ; Dermatitis, Seborrheic ; Fatty Acids ; Fatty Acids, Nonesterified ; Fungi ; Genes, vif ; Genome ; Humans ; Hydrolases ; Lipase ; Malassezia ; Myristic Acid ; Phospholipases

The objective of this study was to compare ovulation rate, number of large ovarian follicles, and concentrations of plasma progesterone (P4) and non-esterified fatty acids (NEFA) between lame (n = 10) and non-lame (n = 10) lactating Holstein cows. The study was conducted in an organic dairy farm, and cows were evaluated by undertaking ultrasonography and blood sampling every 3 days from 30 days postpartum for a period of 34 days. Cows which became lame during the first 30 days postpartum experienced a lower ovulation rate determined by the presence of a corpus luteum (50% presence for lame cows and 100% for non-lame cows, p ≤ 0.05). The number of large ovarian follicles in the ovaries was 5 for lame cows and 7 for non-lame cows (p = 0.09). Compared to non-lame cows, lame cows had significantly lower (p ≤ 0.05) concentrations of plasma P4. Furthermore, NEFA concentrations were lower (p ≤ 0.05) in lame cows than in non-lame cows. It is concluded that lameness in postpartum dairy cows is associated with ovulation failure and lower concentrations of P4 and NEFA.
Agriculture ; Corpus Luteum ; Fatty Acids ; Fatty Acids, Nonesterified ; Female ; Mortuary Practice ; Ovarian Follicle ; Ovary ; Ovulation ; Plasma ; Postpartum Period ; Progesterone ; Ultrasonography

The purpose of this study was to discern the critical point in skeletal muscle fatty acid oxidation by changing plasma free fatty acids (FFA) level in rat. In the study, 3 key steps in lipid oxidation were examined after changing plasma FFA level by acipimox. The rates of both palmitate and palmitoyl- carnitine oxidation were decreased by decrease of plasma FFA level, however, carnitine palmitoyl transferase (CPT) 1 activity was not changed, suggesting CPT1 activity may not be involved in the fatty acid oxidation at the early phase of plasma FFA change. In the fasted rats, beta-hydroxy acyl-CoA dehydrogenase (beta-HAD) activity was depressed to a similar extent as palmitate oxidation by a decrease of plasma FFA level. This suggested that beta-oxidation might be an important process to regulate fatty acid oxidation at the early period of plasma FFA change. Citrate synthase activity was not altered by the change of plasma FFA level. In conclusion, the critical step in fatty acids oxidation of skeletal muscles by the change of plasma FFA level by acipimox in fasting rats might be the beta-oxidation step rather than CPT1 and TCA cycle pathways.
Acyl-CoA Dehydrogenase ; Animals ; Carnitine ; Citrate (si)-Synthase ; Fasting ; Fatty Acids ; Fatty Acids, Nonesterified* ; Muscle, Skeletal ; Plasma* ; Rats* ; Transferases

This study was conducted to evaluate changes in plasma concentration and urinary excretion of carnitine, as well as plasma lipid level and fatty acid composition, caused by short term supplementation of carnitine in humans. Ten healthy male subjects (21.2 +/- 0.5 years old) received oral carnitine supplementation (4 g/day) as tablets for two weeks. Fasting blood and random urine samples were collected from each subject both prior to and at the end of carnitine supplemention program. Following the 2 weeks of carnitine supplementation, plasma total carnitine (TCNE) concentration increased 20% (85.1 +/- 7.4 vs 67.3 +/- 9.1 micro mol/1, p>0.05), while urinary excretion of total carnitine increased ten times compared to the value measured prior to the supplementation (3051 +/- 692 vs 278 +/- 90.1 micro mol/g creatinine, p<0.01). Non-esterified carnitine (NEC) comprised from 71 to 88% of TCNE in plasma, and from 32 to 40% of TCNE excreted in the urine. Two weeks of carnitine supplementation in healthy adults significantly elevated plasma level of acid soluble acylcarnitine (ASAC) which is esterified mostly with short chain fatty acids (21.6 +/- 1.6 micro mol/l) compared to the value measured prior to the supplementation (6.4 +/- 0.8 micro mol/l) (p<0.05). Carnitine supplementation significantly increased plasma HDL-cholesterol level (p<0.05), and decreased the atherogenic index (p<0.05), but failed to cause any significant change in plasma levels of total cholesterol, triglyceride, and free fatty acids. Plasma triglyceride and phospholipid fatty acid compositions were not significaly affected as well by the oral supplementation of carnitine in subjects with normal range of blood lipid levels.
Adult* ; Carnitine* ; Cholesterol ; Creatinine ; Fasting ; Fatty Acids ; Fatty Acids, Nonesterified ; Humans ; Male* ; Plasma* ; Reference Values ; Tablets ; Triglycerides

Pancreatic islets are responsible for blood glucose homeostasis. Reduced numbers of functional (insulin-secreting) beta-cells in pancreatic islets underlies diabetes. Restoration of the secretion of the proper amount of insulin is a goal. Beta-cell mass is increased by neogenesis, proliferation and cell hypertrophy, and is decreased by beta-cell death primarily through apoptosis. Many hormones and nutrients affect beta-cell mass, and glucose and free fatty acid are thought to be the most important determinants of beta-cell equilibrium. A number of molecular pathways have been implicated in beta-cell mass regulation and have been studied. This review will focus on the role of the principle metabolites, glucose and free fatty acid, and the downstream signaling pathways regulating beta-cell mass by these metabolites.
Apoptosis ; Blood Glucose ; Fatty Acids, Nonesterified* ; Glucose* ; Homeostasis ; Hypertrophy ; Insulin ; Islets of Langerhans