Beyond the visible: Accounting for ultraviolet and far-red radiation in vegetation productivity and surface energy budgets.

Photosynthetically active radiation (PAR) is typically defined as light with a wavelength within 400-700 nm. However, ultra-violet (UV) radiation within 280-400 nm and far-red (FR) radiation within 700-750 nm can also excite photosystems, though not as efficiently as PAR. Vegetation and land surface models (LSMs) typically do not explicitly account for UV's contribution to energy budgets or photosynthesis, nor FR's contribution to photosynthesis. However, whether neglecting UV and FR has significant impacts remains unknown. We explored how canopy radiative transfer (RT) and photosynthesis are impacted when explicitly implementing UV in the canopy RT model and accounting for UV and FR in the photosynthesis models within a next-generation LSM that can simulate hyperspectral canopy RT. We validated our improvements using photosynthesis measurements from plants under different light sources and intensities and surface reflection from an eddy-covariance tower. Our model simulations suggested that at the whole plant level, after accounting for UV and FR explicitly, chlorophyll content, leaf area index (LAI), clumping index, and solar radiation all impact the modeling of gross primary productivity (GPP). At the global scale, mean annual GPP within a grid would increase by up to 7.3% and the increase is proportional to LAI; globally integrated GPP increases by 4.6 PgC year-1 (3.8% of the GPP without accounting for UV + FR). Further, using PAR to proxy UV could overestimate surface albedo by more than 0.1, particularly in the boreal forests. Our results highlight the importance of improving UV and FR in canopy RT and photosynthesis modeling and the necessity to implement hyperspectral or multispectral canopy RT schemes in future vegetation and LSMs.

Evidence for persistent UV-induced DNA damage and altered DNA damage response in xeroderma pigmentosa patient corneas.

Xeroderma pigmentosum (XP) is a rare genetic disorder characterized by injury to the ocular surface due to exposure to ultraviolet (UV) radiation. UV-induced damage in the cells leads to the formation of cyclobutane pyrimidine dimers (CPDs) and 6-4 pyrimidine-pyrimidone photoproducts that are repaired by the NER (Nucleotide Excision Repair) pathway. Mutations in the genes coding for NER proteins, as reported in XP patients, would lead to sub-optimal damage repair resulting in clinical signs varying from photo-keratitis to cancerous lesions on the ocular surface. Here, we aimed to provide evidence for the accumulation of DNA damage and activation of DNA repair pathway proteins in the corneal cells of patients with XP. Corneal buttons of patients who underwent penetrating keratoplasty were stained to quantify DNA damage and the presence of activated DNA damage response proteins (DDR) using specific antibodies. Positive staining for pH2A.X and thymidine dimers confirmed the presence of DNA damage in the corneal cells. Positive cells were found in both control corneas and XP samples however, unlike normal tissues, positive cells were found in all cell layers of XP samples indicating that these cells were sensitive to very low levels of UV. pH2A.X-positive cells were significantly more in XP corneas (p < 0.05) indicating the presence of double strand breaks in these tissues. A positive expression of phosphorylated-forms of DDR proteins was noted in XP corneas (unlike controls) such as ataxia telangiectasia mutated/Rad-3 related proteins (ATM/ATR), breast cancer-1 and checkpoint kinases-1 and -2. Nuclear localization of XPA was noted in XP samples which co-localized (calculated using Pearson's correlation) with pATM (0.9 ± 0.007) and pATR (0.6 ± 0.053). The increased presence of these in the nucleus confirms that unresolved DNA damage was accumulating in these cells thereby leading to prolonged activation of the damage response proteins. An increase in pp53 and TUNEL positive cells in the XP corneas indicated cell death likely driven by the p53 pathway. For comparison, cultured normal corneal epithelial cells were exposed to UV-radiation and stained for DDR proteins at 3, 6 and 24 h after irradiation to quantify the time taken by cells with intact DDR pathway to repair damage. These cells, when exposed to UV showed nuclear translocation of DDR proteins at 3 and 6 h which reduced significantly by 24 h confirming that the damaged DNA was being actively repaired leading to cell survival. The persistent presence of the DDR proteins in XP corneas indicates that damage is being actively recognized and DNA replication is stalled, thereby causing accumulation of damaged DNA leading to cell death, which would explain the cancer incidence and cell loss reported in these patients.

Temperature Is a Key Factor Governing the Toxic Impact of Ultra-Violet Radiation-Emitting Nail Dryers When Used on Human Skin Cells.

The skin is the largest organ in the body and the only one to come into contact with solar UV radiation (UVR). UVA (320-400 nm) is a significant contributor to UV-related skin damage. The UVA spectrum makes up over 95% of solar-UV energy reaching the earth's surface causing the majority of the visible signs of skin photoaging. Many consumer products also emit UVA, including nail dryers. There have been sporadic reports suggesting that these units may be contributing to skin cancer incidence. This notion was recently bolstered by a finding that nail dryer-irradiated mammalian skin cells develop a mutational signature consistent with UVA exposure. This report was surprising considering the comparatively low level of UVA to which the skin is exposed during nail treatments. In this research, we investigated how UVA-emitting devices caused cytotoxic/genotoxic impact after only low levels of UVA exposure. Our data showed that levels of UVA in the unit are highly variable and location dependent. We confirm previous reports that using prolonged exposure protocols could induce significant levels of DNA damage. It was also determined that UV-induced DNA damage only partially correlated with the level of UVA fluency. On investigation, we found that the unit had a rapid increase in internal temperature when in use. Exposing human cells to these elevated temperatures acted synergistically with UVA to magnify the cytotoxic and genotoxic impact of UV irradiation.

Visible light and human skin pigmentation: The importance of skin phototype.

Melanin is synthesised within melanocytes and transferred to keratinocytes in human skin, thereby regulating skin colour and protecting skin cells against UVR-induced damage. We commonly divide human skin into six phototypes (SPT)-I to -VI (Fitzpatrick scale) according to the skin's tanning response to UVR. In this pilot study, we investigated the impact of UVR (maximum 311nm), blue (peak 450nm) and green visible light (peak 530nm) on melanin production and type in healthy human skin histocultures (SPT-I, -II and -III). UVR, blue and green light stimulated a surface tanning response in SPT-II and -III, but not SPT-I. Using the Warthin-Starry stain for sensitive melanin detection, all three light treatments induced melanogenesis in SPT-II and -III skin. Surprisingly, blue and green light (but not UVR) stimulated melanin synthesis in SPT-I skin. Moreover, melanin synthesis induced by blue and green visible light in SPT-I, SPT-II, and SPT-III skin was not associated with a detectable increase in DNA damage or cell apoptosis. By contrast, both responses were detected after UVR. These data suggest that blue and green visible light can stimulate melanin production in fair-skinned individuals without, at least some of, the harmful consequences of UVR-induced pigmentation. We are currently examining the molecular basis of UVR-independent melanogenesis in fair skin.

Vitamin D and UV exposure in construction workers-a randomized control trial using text messaging to promote positive behaviours.

BACKGROUND: The aim of this study was to determine whether a text messaging intervention (supported by a smartphone application) would be effective in the promotion of sun-safe behaviours. Both excessive and insufficient exposure to ultra-violet (UV) radiation were considered. METHODS: A randomized control crossover trial was conducted. 112 participants from nine sites in the United Kingdom contributed to the study. There were three intervention waves, two in winter (Vitamin D-focussed) and one in summer (UV exposure-focussed). Stages of Change, Standard Erythemal (UV) Dose and assayed blood samples (Vitamin D) were employed to evaluate the effectiveness throughout the 21-day data collection periods. RESULTS: The intervention was effective in promoting positive progression in Stages of Change for Vitamin D; and this in turn was predictive of increased Vitamin D levels in participants. More limited positive findings were found with respect to UV exposure. Overall, for those in the Intervention, Vitamin D levels were significantly predicted to increase during both of the winter data collection waves. CONCLUSIONS: Interventions of this type are recommended to promote healthy Vitamin-D levels in construction workers.

microRNA-4532 inhibition protects human lens epithelial cells from ultra-violet-induced oxidative injury via activating SIRT6-Nrf2 signaling.

Ultra-violet radiation (UVR) can induce significant oxidative injury to human lens epithelial cells (HLECs). Sirtuin 6 (SIRT6) is shown to directly bind to Nrf2, essential for Nrf2 signaling activation. In the present study, we show that microRNA-4532 (miR-4532) targets SIRT6 to regulate Nrf2 signaling in HLECs. Ectopic overexpression of miR-4532 in HLECs decreased SIRT6 3'-UTR activity, causing SIRT6 downregulation and Nrf2 signaling inhibition. Conversely, miR-4532 inhibition, by a lentiviral construct, enhanced SIRT6 3'-UTR activity, SIRT6 expression and Nrf2 signaling activation. Functional studies show that UVR-induced cytotoxicity and apoptosis in HLECs were potentiated by miR-4532 overexpression, Nrf2 depletion or SIRT6 shRNA. Conversely, miR-4532 inhibition or ectopic SIRT6 overexpression attenuated UVR-induced oxidative injury in HLECs. Importantly, miR-4532 overexpression or inhibition was ineffective in SIRT6-KO or Nrf2-KO HLECs. Taken together, the results show that inhibition of miR-4532 protects HLECs from UVR-induced oxidative injury via activation of SIRT6-Nrf2 pathway. Targeting the miR-4532-SIRT6-Nrf2 pathway could be a novel strategy to protect HLECs from UVR and possible other oxidative stresses.

Decontamination of poultry feed from ochratoxin A by UV and sunlight radiations.

BACKGROUND: Mycotoxin-contaminated feed is very dangerous for the growth and even life of poultry. The objective of the current study was to investigate the efficacy of ultra-violet irradiation for decontamination of ochratoxin A (OTA) in spiked and naturally contaminated poultry feed samples. Spiked and naturally contaminated feed samples were irradiated with ultra-violet light (UV) at distance of 25 cm over the feed samples. In vitro, the effect of UV intensity (0.1 mW cm(-2) at 254 nm UV-C) on different types of poultry feeds contaminated with OTA was evaluated. The same samples were also irradiated with sunlight and analysed for OTA by an indirect enzyme linked immunosorbent assay method. RESULTS: Poultry feed samples containing 500 µg kg(-1) were 100% decontaminated in 180 min with UV radiation while OTA was decreased to 70-95 µg kg(-1) using the same poultry feed samples after 8 h sunlight irradiation. Therefore, UV light was found to be more effective. Only 1 h of UV irradiation was found to be sufficient to bring the OTA level to the maximum regulatory limit suggested for poultry feeds (100 µg kg(-1) ), while 8 h were needed to obtain this level using sunlight radiations. CONCLUSION: The proposed approach is a viable option to reduce the level of OTA in contaminated poultry feeds. © 2015 Society of Chemical Industry.

Review on interactions between nanomaterials and phytohormones: Novel perspectives and opportunities for mitigating environmental challenges.

Nanotechnology offers the potential to provide innovative solutions for sustainable crop production as plants are exposed to a combination of climate change factors (CO2, temperature, UV radiation, ozone), abiotic (heavy metals, salinity, drought), and biotic (virus, bacteria, fungi, nematode, and insects) stresses. The application of particular sizes, shapes, and concentration of nanomaterials (NMs) potentially mitigate the negative impacts in plants by modulation of photosynthetic rate, redox homeostasis, hormonal balance, and nutrient assimilation through upregulation of anti-stress metabolites, antioxidant defense pathways, and genes and genes network. The present review inculcates recent advances in uptake, translocation, and accumulation mechanisms of NMs in plants. The critical theme of this review provides detailed insights into different physiological, biochemical, molecular, and stress tolerance mechanism(s) of NMs action and their cross-talk with different phytohormones. The role of NMs as a double-edged sword for climate change factors, abiotic, and biotic stresses for nutrients uptake, hormones synthesis, cytotoxic, and genotoxic effects including chromosomal aberration, and micronuclei synthesis have been extensively studied. Importantly, this review aims to provide an in-depth understanding of the hormesis effect at low and toxicity at higher doses of NMs under different stressors to develop innovative approaches and design smart NMs for sustainable crop production.

Effect of Poling on Photocatalysis, Piezocatalysis, and Photo-Piezo Catalysis Performance of BaBi4Ti4O15 Ceramics.

This study focuses on analyzing the poling effect of BaBi4Ti4O15 (BBT) on the basis of photo and piezo-catalysis performance. BBT powder is prepared via a solid state reaction followed by calcination at 950 °C for 4 h. BBT is characterized by an X-ray diffractometer, scanning electron microscopy, Raman spectroscopy, and X-ray photoelectron spectroscopy. The optical bandgap of BBT is evaluated with the help of Tauc's plot and found to be 3.29 eV, which comes in the photon energy range of ultra-violet radiation. BBT powder is poled by using Corona poling in the presence of 2 kV mm-1 of electric field. An aqueous solution of methyl blue (MB) dye in the presence of UV radiation is used to evaluate the photo/piezocatalysis performance. Photocatalysis, piezocatalysis, and photo-piezo catalysis degradation efficiencies of poled and unpoled BBT powder are tested for 120 min of UV light irradiation. Photo-piezocatalysis shows degradation efficiencies of 62% and 40% for poled and unpoled BBT powder, respectively. Poling of BBT powder shows significant enhancement in degradation performance of MB dye in aqueous solution. Scavenger tests are also performed to identify reactive species.

Topical Iron Chelator Therapy: Current Status and Future Prospects.

Systemic iron chelation therapy has long been used for iron overload, providing a role in returning iron levels to proper homeostatic concentrations. Recently, topical iron chelation therapy has emerged as a potential strategy for treating skin damage. This narrative review explores the current status and future prospects of topical iron chelation therapy for treating ultraviolet (UV) and non-UV skin damage, as well as its potential application in wound healing. The review was conducted through a literature search across PubMed, Web of Science, and EMBASE databases, spanning publications from 1990 to 2023. The selection of articles was focused on primary research studies, either experimental or clinical, that explored the implications and formulations of topical iron chelators used alone or in conjunction with another therapeutic agent. The search strategy employed a combination of terms, including "topical iron chelation", "topical deferoxamine", "UV", "wound healing", "skin inflammation", "radiation-induced fibrosis", and "skin cancer". Relevant studies, including methods, intervention strategies, measured outcomes, and findings, are summarized. The review also considered the potential challenges in translating research findings into clinical practice. Results indicate that topical iron chelators, such as deferoxamine, are effective in mitigating UV-induced skin damage, reducing tumorigenesis, and decreasing oxidative damage. In addition, the use of these agents in radiation-induced fibrosis has been shown to significantly increase skin elasticity and reduce dermal fibrosis. Several studies also highlight the use of topical iron chelators in difficult-to-treat chronic wounds, such as diabetic neuropathic ulcers and sickle cell ulcers. In conclusion, topical iron chelation therapy represents a novel and promising approach for skin protection and wound healing. Its potential makes it a promising area of future research.

Sun protection and occupation: Current developments and perspectives for prevention of occupational skin cancer.

A substantial proportion of all reported occupational illnesses are constituted by skin cancer, making this disease a serious public health issue. Solar ultra-violet radiation (UVR) exposure is the most significant external factor in the development of skin cancer, for which the broad occupational category of outdoor workers has already been identified as high-risk group. Sun protection by deploying adequate technical, organizational, and person-related measures has to be understood as a functional aspect of workplace safety. To prevent skin cancers brought on by-typically cumulative-solar UVR exposure, outdoor workers must considerably lower their occupationally acquired solar UVR doses. Estimating cumulative sun exposure in outdoor workers requires consideration of the level of solar UVR exposure, the tasks to be done in the sun, and the employees' solar UVR preventive measures. Recent studies have highlighted the necessity for measures to enhance outdoor workers' sun protection behavior. In the coming decades, occupational dermatology is expected to pay increasing attention to sun protection at work. Also, the field of dermato-oncology will likely be concerned with sky-rocketing incidences of occupational skin cancers. The complete range of available alternatives should be utilized in terms of preventive actions, which seems pivotal to handle the present and future challenges in a purposeful manner. This will almost definitely only be possible if politicians' support is effectively combined with communal and individual preventive actions in order to spur long-term transformation.

Regional Variation in Epidermal Susceptibility to UV-Induced Carcinogenesis Reflects Proliferative Activity of Epidermal Progenitors.

To better understand the influence of ultraviolet (UV) irradiation on the initial steps of skin carcinogenesis, we examine patches of labeled keratinocytes as a proxy for clones in the interfollicular epidermis (IFE) and measure their size variation upon UVB irradiation. Multicolor lineage tracing reveals that in chronically irradiated skin, patches near hair follicles (HFs) increase in size, whereas those far from follicles do not change. This is explained by proliferation of basal epidermal cells within 60 µm of HF openings. Upon interruption of UVB, patch size near HFs regresses significantly. These anatomical differences in proliferative behavior have significant consequences for the cell of origin of basal cell carcinomas (BCCs). Indeed, a UV-inducible murine BCC model shows that BCC patches are more frequent, larger, and more invasive near HFs. These findings have major implications for the prevention of field cancerization in the epidermis.

Integrity of the DNA and Cellular Ultrastructure of Cryptoendolithic Fungi in Space or Mars Conditions: A 1.5-Year Study at the International Space Station.

The black fungi Cryomyces antarcticus and Cryomyces minteri are highly melanized and are resilient to cold, ultra-violet, ionizing radiation and other extreme conditions. These microorganisms were isolated from cryptoendolithic microbial communities in the McMurdo Dry Valleys (Antarctica) and studied in Low Earth Orbit (LEO), using the EXPOSE-E facility on the International Space Station (ISS). Previously, it was demonstrated that C. antarcticus and C. minteri survive the hostile conditions of space (vacuum, temperature fluctuations, and the full spectrum of extraterrestrial solar electromagnetic radiation), as well as Mars conditions that were simulated in space for a 1.5-year period. Here, we qualitatively and quantitatively characterize damage to DNA and cellular ultrastructure in desiccated cells of these two species, within the frame of the same experiment. The DNA and cells of C. antarcticus exhibited a higher resistance than those of C. minteri. This is presumably attributable to the thicker (melanized) cell wall of the former. Generally, DNA was readily detected (by PCR) regardless of exposure conditions or fungal species, but the C. minteri DNA had been more-extensively mutated. We discuss the implications for using DNA, when properly shielded, as a biosignature of recently extinct or extant life.

Phosphate oxygen isotope evidence for methylphosphonate sources of methane and dissolved inorganic phosphate.

The ocean is an important source of methane, however, the sources of oceanic methane and mechanisms of its release to the atmosphere have only recently begun to be understood. Recent studies have identified methylphosphonate (MPn) as a previously unknown and likely source of methane in the aerobic ocean (Karl et al., 2008), as well as shown the biosynthesis of methylphosphonic acid to be a widespread trait in marine microbes (Metcalf et al., 2012). The mechanisms and reaction pathways from MPn to free methane, however, have not been well studied. Here we present results of laboratory studies on the photo-degradation of MPn, a likely mechanism of methane release to the atmosphere and phosphate release to the surface oceans. Phosphonoacetic acid was also studied as an additional model compound for comparison. We used the multi-labeled water isotope probing (MLWIP) approach, involving 18O-labeled waters to probe the photolytic mechanism of CP bond cleavage in phosphates through analysis of P released from MPn as PO4. These studies identified distinct reaction pathways involving phosphates compared with other common organophosphorus compounds (e.g., phosphoesters), as well as suggest the involvement of both ambient water and atmospheric oxygen in CP bond cleavage. There is only a small amount of water oxygen incorporated into product PO4 after cleavage of the CP bond in MPn, suggesting atmospheric O2 or radicals formed from O2 under Ultra Violet Radiation (UVR), as the primary source of O that replaces C in the CP bond of MPn. Model calculations suggest that the δ18OP signature of phosphate released via UV-degradation of phosphates is largely (75%) inherited from the original phosphate substrate. This opens up the possibility of tracing and differentiating specific phosphate sources of dissolved phosphate from other organophosphorus (Porg) sources (e.g., phosphoesters) used in primary production, as well as for tracing specific MPn sources of atmospheric methane.

DNA Fiber Assay upon Treatment with Ultraviolet Radiations.

Genome stability is continuously challenged by a wide range of DNA damaging factors. To promote a correct DNA repair and cell survival, cells orchestrate a coordinated and finely tuned cascade of events collectively known as the DNA Damage Response (DDR). Ultra Violet (UV) rays are among the main environmental sources of DNA damage and a well recognized cancer risk factor. UV rays induce the formation of toxic cyclobutane-type pyrimidine dimers (CPD) and [6-4]pyrimidine-pyrimidone (6-4PP) photoproducts which trigger the activation of the intra-S phase cell cycle checkpoint (Kaufmann, 2010) aimed at preventing replication fork collapse, late origin firing, and stabilizing fragile sites (Branzei and Foiani, 2009). To monitor the activation of the intra-S phase checkpoint in response to UV type C (UVC) exposure, the DNA fiber assay can be used to analyse the new origin firing and DNA synthesis rate ( Jackson et al., 1998 ; Merrick et al., 2004 ; Alfano et al., 2016 ). The DNA fiber assay technique was conceived in the 90s and then further developed through the use of thymidine analogues (such as CldU and IdU), which are incorporated into the nascent DNA strands. By treating the cells in sequential mode with these analogues, which can be visualized through specific antibodies carrying different fluorophores, it is possible to monitor the replication fork activity and assess how this is influenced by UV radiations or others agents.

Off-target response of a Wip1 chemical inhibitor in skin keratinocytes.

BACKGROUND: The wild type p53 inducible phosphatase (Wip1) plays an important role in modulating not only stress responses by various environmental stresses, but when overexpressed it also impairs the intrinsic tumor surveillance networks that are frequently found in a number of cancers including skin cancers. As a result, using a pharmacological inhibitor of Wip1 has been suggested to be a novel chemotherapeutic approach to recover the innate tumor surveillance in a variety of cancers. OBJECTIVE: We studied the effect of a pharmacological inhibitor of Wip1 in skin keratinocytes, under a ultra-violet (UV) stress condition. METHODS: A human keratinocyte cell line or human epidermal keratinocytes were exposed to UV, with or without the sole commercially available chemical inhibitor of Wip1, CCT007093; subsequently, we determined the diverse stress responses, including apoptosis and the activation of stress signaling. RESULTS: We demonstrate that the Wip1 inhibitor unexpectedly attenuated the UV-mediated apoptotic response in skin keratinocytes, as a consequence of attenuated JNK activation and reduced H2AX phosphorylation in both, skin keratinocytes and a Wip1-null cell model. On the other hand, the loss of Wip1 expression, either by knockout or knockdown in mice or human keratinocytes respectively, promoted apoptosis and potentiated H2AX phosphorylation following UV treatment. Of note, CCT007093 treatment appeared to promote apoptosis in breast cancer cells and skin transformed keratinocytes that ectopically expressed Wip1, demonstrating that the effect of CCT007093 differs based on the level of Wip1 expression. CONCLUSION: Thus, our studies suggest that the development of a more potent and specific Wip1 inhibitor is necessary to achieve the desired chemotherapeutic potential and to avoid off-target effects.

Evaluating sanitization of toothbrushes using ultra violet rays and 0.2% chlorhexidine solution: A comparative clinical study.

BACKGROUND: Toothbrushes may play a significant role in plaque control. Toothbrushes should be correctly stored, disinfected and changed at regular intervals. OBJECTIVE: The purpose of this study was to evaluate the efficacy of 0.2% chlorhexidine (CHX) gluconate solution and ultra violet (UV) toothbrush-sanitizer for toothbrush disinfection. MATERIALS AND METHODS: Fresh tooth brushes were distributed to fifteen study subjects, who were selected randomly and who met the study criteria. All the study participants were asked to brush their teeth with the tooth brush provided. No special instructions were given regarding the brushing techniques. Toothbrushes were collected after 7 days. All tooth brushes were randomly allocated to three groups. Tooth brushes were subjected to microbial analysis and total bacterial count was assessed. Tooth brushes allocated to Group I were soaked in 2% CHX mouthwash for 12 h, Group II were kept in UV-light toothbrush holder for 7 min, and Group III were soaked in normal saline for 12 h. All the toothbrushes were subjected for microbial analysis and mean bacterial count was determined. RESULTS: There was a statistically significant difference between mean colony-forming unit count pre-sanitization and post-sanitization in all the groups, using 0.2% CHX gluconate, UV rays and normal saline (P < 0.007). However, the mean bacterial count reduced drastically after the treatment with UV rays (P = 0.001). CONCLUSIONS: CHX, UV rays and normal saline are effective in a reduction of bacterial count on toothbrushes. UV rays treatment was more effective, when compared to CHX and normal saline.

Autophagy and apoptosis dysfunction in neurodegenerative disorders.

Autophagy and apoptosis are basic physiologic processes contributing to the maintenance of cellular homeostasis. Autophagy encompasses pathways that target long-lived cytosolic proteins and damaged organelles. It involves a sequential set of events including double membrane formation, elongation, vesicle maturation and finally delivery of the targeted materials to the lysosome. Apoptotic cell death is best described through its morphology. It is characterized by cell rounding, membrane blebbing, cytoskeletal collapse, cytoplasmic condensation, and fragmentation, nuclear pyknosis, chromatin condensation/fragmentation, and formation of membrane-enveloped apoptotic bodies, that are rapidly phagocytosed by macrophages or neighboring cells. Neurodegenerative disorders are becoming increasingly prevalent, especially in the Western societies, with larger percentage of members living to an older age. They have to be seen not only as a health problem, but since they are care-intensive, they also carry a significant economic burden. Deregulation of autophagy plays a pivotal role in the etiology and/or progress of many of these diseases. Herein, we briefly review the latest findings that indicate the involvement of autophagy in neurodegenerative diseases. We provide a brief introduction to autophagy and apoptosis pathways focusing on the role of mitochondria and lysosomes. We then briefly highlight pathophysiology of common neurodegenerative disorders like Alzheimer's diseases, Parkinson's disease, Huntington's disease and Amyotrophic lateral sclerosis. Then, we describe functions of autophagy and apoptosis in brain homeostasis, especially in the context of the aforementioned disorders. Finally, we discuss different ways that autophagy and apoptosis modulation may be employed for therapeutic intervention during the maintenance of neurodegenerative disorders.

Towards a critical understanding of the photosystem II repair mechanism and its regulation during stress conditions.

Photosystem II (PSII) is vulnerable to high light (HL) illumination resulting in photoinhibition. In addition to photoprotection mechanisms, plants have developed an efficient PSII repair mechanism to save themselves from irreversible damage to PSII under abiotic stresses including HL illumination. The phosphorylation/dephosphorylation cycle along with subsequent degradation of photodamaged D1 protein to be replaced by the insertion of a newly synthesized copy of D1 into the PSII complex, is the core function of the PSII repair cycle. The exact mechanism of this process is still under discussion. We describe the recent progress in identifying the kinases, phosphatases and proteases, and in understanding their involvement in the maintenance of thylakoid structure and the quality control of proteins by PSII repair cycle during photoinhibition.

Potential of herbs in skin protection from ultraviolet radiation.

Herbs have been used in medicines and cosmetics from centuries. Their potential to treat different skin diseases, to adorn and improve the skin appearance is well-known. As ultraviolet (UV) radiation can cause sunburns, wrinkles, lower immunity against infections, premature aging, and cancer, there is permanent need for protection from UV radiation and prevention from their side effects. Herbs and herbal preparations have a high potential due to their antioxidant activity, primarily. Antioxidants such as vitamins (vitamin C, vitamin E), flavonoids, and phenolic acids play the main role in fighting against free radical species that are the main cause of numerous negative skin changes. Although isolated plant compounds have a high potential in protection of the skin, whole herbs extracts showed better potential due to their complex composition. Many studies showed that green and black tea (polyphenols) ameliorate adverse skin reactions following UV exposure. The gel from aloe is believed to stimulate skin and assist in new cell growth. Spectrophotometer testing indicates that as a concentrated extract of Krameria triandra it absorbs 25 to 30% of the amount of UV radiation typically absorbed by octyl methoxycinnamate. Sesame oil resists 30% of UV rays, while coconut, peanut, olive, and cottonseed oils block out about 20%. A "sclerojuglonic" compound which is forming from naphthoquinone and keratin is the reaction product that provides UV protection. Traditional use of plant in medication or beautification is the basis for researches and making new trends in cosmetics. This review covers all essential aspects of potential of herbs as radioprotective agents and its future prospects.