Zeichner also suggests this drugstore find which "combines citric and glycolic acid with a soy and kiwi complex to exfoliate and brighten the skin. Since , I've been applying this light-weight, clear gel to my face to keep my oily skin in check. A combination of lactic and glycolic acids increases cell turnover, which reduces blackheads, pore size and dark spots.
She continues that gluconolactone is an exfoliant that results in a smoother and brighter complexion. However, unlike AHAs, it is a humectant, which means it helps skin hold onto water. She also recommends that her patients, including those with sensitive skin, use this peel twice a week. Maiman also recommends this face cream for oily and acne-prone skin, which can be used up to twice daily.
It contains four AHAs -- lactic, glycolic, citric and malic acids -- and salicylic acid, a popular acne-fighting ingredient classified as a BHA. There's tocopheryl acetate, "a stabilized form of vitamin E," and pro-vitamin B5, both of which are humectants and emollients, "which makes them great at combating the dryness and irritation that can be caused by the use of hydroxy-acids. Maiman calls this night cream "pretty revolutionary" because it contains lactic acid and topical retinoid, two "potent" anti-aging ingredients.
She says the formula of the cream is "chemically stable" and non-irritating. Maiman continues that when you apply the cream, your skin's water content will trigger a slow release of each active ingredient, making it less irritating to the skin, "though it is no less effective. IE 11 is not supported. For an optimal experience visit our site on another browser. Follow Select. By Nicole Saunders.
That process will result in less hyperpigmentation and more even-toned skin Cheung says AHAs "offer almost instant gratification" and they're suitable for someone who wants to "refresh" their skin.
Shopping 12 Best spray sunscreens of The fruit acids in the AHA family, like citric and malic, are considered to be the gentlest of the bunch because of their larger molecular size and tend to do their best work when paired with their stronger counterparts, glycolic and lactic acid. Most people — even those with sensitive skin — can use alpha hydroxy acids as long as they're approached wisely. However, don't rush in. Hirsch adds. Not everyone should aim to use AHAs daily, though.
Markowitz says that especially dry skin types should avoid using them, ironically because of their humectant abilities. Rabach also cautions against using alpha hydroxy acids on irritated, damaged think wounds, cuts, and sunburns , and eczema-prone skin. There are numerous ways to incorporate alpha hydroxy acids into your at-home regimen. You'll find all kinds of AHAs in creams and serums. Many daily-use cleansers contain AHAs, though usually not at particularly potent levels. Courtesy of brand.
To avoid irritation if you opt for a cream or serum, Dr. Rabach echoes Dr. Hirsch's advice for a cautious approach, recommending a slow and steady pace when introducing alpha hydroxy acids to your skin-care routine.
You'll also want to pay attention to the acid percentage in your chosen products. Rabach says. The Cosmetic Ingredient Review says that it's safe to regularly use products with glycolic or lactic acid concentrations of 10 percent or less. Percentage isn't the only thing to consider, there's also pH. CA and MA play different roles in relation to skin cells.
One study found that CA induced collagen I and procollagen II proliferation and GA improved the epidermis and dermis, thereby verifying the usefulness of AHAs for rejuvenating photo-damaged skin [ 25 ]. CA has also been found to increase the skin renewal rate [ 26 ] and treat sun-damaged skin.
These functions may correlate with promoting keratinocyte apoptosis. Apoptosis also called programmed cell death can be activated through two main pathways: the mitochondria-dependent pathway intrinsic pathway and the death-receptor-dependent pathway extrinsic pathway [ 27 ]. The Fas receptor, Fas ligand, and caspase-8 are parts of an important cellular pathway that regulates the induction of apoptosis in diverse cell and tissue types [ 28 ]. We investigated the regulatory function of CA in skin cells.
HaCaT is an excellent model to investigate the keratinocyte system in vitro [ 29 ]. HaCaT keratinocytes were derived from a histologically normal skin biopsy at the far periphery of a male melanoma patient [ 30 ]. Although HaCaT cells have intrinsic differences e.
We found that CA We clarified that CA also activated death receptors, increased the level of caspase-8, and activated the BH3-interacting domain death agonist BID protein, apoptosis-inducing factor, and endonuclease G Endo G. CA induces apoptosis through the mitochondrial pathway in HaCaT cells [ 15 ]. These mechanisms could cause an increase in the skin renewal rate. We summarized that MA-induced apoptosis was found to occur through two molecular pathways: i endoplasmic reticulum stress and ii mitochondria-dependent signaling pathways [ 16 ].
Despite the structural differences between CA and MA, these two compounds activate the same apoptotic pathways. After treatment with CA or MA, HaCaT cells exhibit the apoptotic features of DNA damage, apoptotic bodies, and an increase of sub-G1 cells, all of which are due to the activation of caspase-8, -9, and -3 from mitochondria. Molecular pathways involved in the effects of citric acid and malic acid on HaCaT cells.
Citric acid inhibits the proliferation of HaCaT cells via the induction of cell-cycle arrest and apoptosis.
Summarizing our previous studies evaluating the effects of treatment with citric acid or malic acid, HaCaT cells exhibit the apoptotic features of apoptotic bodies, DNA damage, and an increase of sub-G1 cells, resulting from activation of caspase-8, -9, and -3 and the induction of AIF and endonuclease G Endo G release from mitochondria. Citric acid CA and malic acid MA -induced apoptosis occur through multiple molecular pathways including the involvement of endoplasmic reticulum ER stress- and mitochondria-dependent signaling pathways.
Red arrows indicate up-regulation; blue arrows indicate down-regulation. ROS: reactive oxygen species. CA has been found to increase the skin renewal rate, which could correlate with inducing keratinocyte apoptosis.
Recently studies have explored the efficacy of MA for treating Listeria monocytogenes in the skin, and suggest that MA has antibacterial function [ 32 ]. Additionally, the findings of Yamamoto et al. These new findings demonstrate that MA and CA have more diverse biological functions in skin cells. Smith et al. This may be a result of the presence of LA and LA bacteria in the gut and skin. LA also contributes to the cell cycle in human keratinocytes.
We demonstrated that LA at 7. Recently, LA and probiotics have once again become prominent through participation in the microbiome research boom.
Human clinical trials clearly suggest that probiotic supplementation might be beneficial to the skin [ 34 ]. LA maintains intestinal microflora through acid-based balancing properties [ 35 ]. Accumulating evidence suggests that intestinal microbiota correlate with many health issues such as obesity, diabetes, metabolic syndrome, inflammatory bowel disease, autoimmune disease, colon cancer, and atopic dermatitis AD [ 36 ].
In one example, Bifidobacterium longum sp. SP is abundant in the skin [ 37 ] and the gut [ 38 ], and acts as a transmitter in the bidirectional gut—skin communication network. SP is an undecapeptide of the tachykinin family. In the skin, SP is considered a major mediator of inflammation.
SP contributes to the pathogenesis of numerous skin diseases, such as psoriasis, AD, and acne [ 39 ]. SP-regulated LA release may be involved in maintaining the anti-inflammatory status of the skin, and LA may also play a role in gut—skin immunoregulation.
LA and GA are two ingredients that have been familiar to the cosmetic and dermatological community for many years. The two types of LA have been verified as equally effective for increasing cell renewal function. Overall, regarding the roles of AHAs in the biological responses of skin cells, we clarified that at indicated concentrations, CA, MA, and LA all induced cell death in the immortalized HaCaT cell line [ 15 , 16 , 17 ].
Furthermore, AHA-induced apoptosis occurred through multiple molecular pathways, including caspase-dependent and caspase-independent pathways. These results revealed that AHAs induce cell death in keratinocyte cells, and this evidence expands our knowledge of the function of AHAs in skin cells.
A variety of acids can stimulate skin cell renewal, have the potential to irritate the skin, and can provide long-term cosmetic benefits such as improvements in skin firmness and elasticity and the reduction of lines and wrinkles. Some have suggested that the answer lies in the ability of AHAs to increase skin cell renewal. A well-known major cause of skin aging is chronic microinflammation triggered by UV irradiation and external pollutants [ 41 ].
Many studies have demonstrated that peeling can increase the sensitivity of the skin to UV light, and even more have indicated that UV light combined with AHA-associated peeling leads to more serious skin damage [ 7 ]. Lask et al. However, some studies have asserted the opposite view. Davidson and Wolfe considered chemical peeling and dermabrasion able to counteract to some degree the premature UV-aging of skin from chronic actinic damage [ 42 ].
People live in a sunny environment, and those undergoing peeling cannot completely avoid sun exposure. To determine the optimal level of peeling, measurement of UV-light-induced damage in affected patients could provide valuable information on the clinical significance of the effects of AHAs on the skin.
In clinics, the typical measurements used to assess UV damage are decreased minimal erythemal dose MED , increased tanning, and increased formation of SBCs [ 43 ]. However, many individual differences in peeling concentrations can be observed. Thus, further cell-based experiments must be conducted to obtain more detailed information. In the context of the epidermis, the acidic nature of AHAs reduces the pH, inhibits transferases and kinases, and interferes with the formation of ionic bonds, all of which contribute to desmosome resolution and stimulate desquamation.
The possible complications due to chemical peeling are postinflammatory hyperpigmentation, infections, scarring, allergic reactions, milia, persistent erythema, and textural changes. Antoniou et al. The intensity of GA peeling is determined by the concentration of the acid [ 3 ]. The U. FDA has recommended exercising caution in relation to adverse reactions such as redness, swelling, burning, and pruritus due to use of AHA-containing products [ 44 ].
The Ministry of Health and Welfare, R. However, further caution is recommended regarding the effects of AHAs on the epidermis and dermis, as well as the interrelationships between these effects and concentration and pH. AHAs and the skin: friend or foe? Whether AHAs enhance or decrease photo damage of the skin remains unclear. GA is often used to treat acne, normalize keratinization, and decrease epidermal thickness, dermal hyaluronic acid, and collagen gene expression [ 46 ].
Similarly, varying views regarding this question have been expressed. However, our findings are contradictory to those of Ahn et al. These conflicting results indicate that whether GA is a friend or foe of skin cells may depend on its concentration. This turning point led our laboratory members to believe that GA may exert different effects at different concentrations. We employed high 5 mM; pH 7. The contradictory data obtained in HaCaT cells with GA depended on the concentrations and intrinsic property of these compounds, indicating that GA may have an anti-inflammatory effect via epigenetic modifications at low concentrations, whereas GA at high concentrations had a synergistic phototoxic effect on HaCaT keratinocytes.
GA at high concentrations will disrupt the cohesion of skin barrier corneocytes, and results in skin irritation or peeling, which will exacerbate photodamage of the skin.
UV irradiation induces multiple cell responses, such as ROS accumulation, cell apoptosis, DNA breakage and damage, cell cycle arrest, and inflammasome formation [ 48 ]. Regarding these notable features, we found that GA at a low concentration 0.
We demonstrated that GA at a low concentration 0. These results all indicate that GA at a low concentration 0. Our study clarified that GA at a low concentration 0. Glycolic acid GA had anti-inflammatory and photoprotective effects against UVB-irradiation in keratinocytes. Left UVB-irradiation activated the nuclear factor-kappa B NF-kB pathway and promoted the inflammasome complex assembly, which in ROS accumulation and the release of several proinflammatory cytokines e. All of the proinflammatory cytokines were significantly stimulated in UVB-irradiated keratinocytes.
These released cytokines also need other cells e. These questions will need more research in the future. We suggest that GA is a friend of the skin at low concentrations because of its protection against UVB. These data are sufficient to explain that the ability of GA to enhance or decrease photo damage to the skin is dependent on its concentration.
Similar results can be found throughout the literature. Hong et al. The concentration of GA used in these experiments was higher than that used in our animal model.
However, some factors should be considered, such as the skin smear area, GA volume, adjuvant, and animal strain. The influence of these factors needs to be considered. To better understand GA at various concentrations 0. Review of the various biological effects phototoxicity or photoprotection and mechanisms apoptosis or anti-inflammation of GA on human keratinocytes HaCaT or NHEK , and in the mice animal model.
Currently, a considerable volume of research and noteworthy literature on the photoprotective and anti-inflammatory effects of AHAs is available.
However, the photoprotective activity is dependent on the amounts of these compounds that reach the viable skin layers. Chemical movement across the skin cell membrane can occur via channel, diffusion, and receptor [ 54 ]. Some studies have indicated that the vanilloid-receptor-related transient receptor potential TRPV family is a type of AHA receptor [ 55 ].
AQP-3 protein expressed in the basal layer of the epidermis, and a deficiency of AQP3 reduces stratum corneum hydration [ 56 ].
We also intend to explore whether GA as a water repellent avoids UVB irradiation and causes dehydration.
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