Peroxynitrite (PN, ONOO-), formed by nitric oxide radical (•NO) and superoxide radical (O2•-), plays an important role in post-traumatic oxidative damage. In the early work, we determined the temporal characteristics of PN-derived oxidative damage in a rat spinal cord injury (SCI) model. Our results showed 3-nitrotyrosine (3-NT), a specific marker for PN, rapidly accumulated at early time points (1 hr, 3 hrs), after when it plateaued and the high level was sustained to 1 week post injury. The co-localization of 3-NT and lipid peroxidation derived-4-HNE observed in immunohistochemistry indicates PN is involved in lipid peroxidative as well as protein nitrative damage. PN-oxidative damage exacerbates intracellular Ca2+ overload, which activates Ca2+ dependent calpain-mediated cytoskeletal protein (α-spectrin) degradation. The 145 kD fragments of α-spectrin (SBDP 145), which are specifically generated by calpain, increased dramatically as early as 1 hr after injury although the peak increase did not occur until 72 hrs post injury. The high level waned back toward sham level at one week post injury. We then carried out experiments to evaluate the beneficial effects of tempol, a scavenger of PN-derived radicals, following SCI. Three pathological events including PN-induced oxidative damage, mitochondrial dysfunction and cytoskeletal degradation were investigated. Immunoblotting and immunohistochemical studies indicated PN-mediated oxidative damage including protein nitration, protein oxidation and lipid peroxidation, were all reduced by a single dose of tempol (300mg/kg, i.p) after SCI. Spinal cord (SC) mitochondrial dysfunction in terms of the respiratory control ratio (RCR) significantly improved by both 150 mg/kg and 300 mg/kg tempol treatments. Moreover, calpain-mediated proteolysis was significantly decreased by tempol, with greater effects on calpain-specific SBDP 145 observed. Direct PN-scavenging effect of tempol was confirmed in vitro. Exposure of healthy SC mitochondria to SIN-1, a PN donor in vitro, impaired mitochondrial respiration in a dose-dependent manner. Tempol was able to protect mitochondria against SIN-1-induced damage by improving mitochondrial function and decreasing mitochondrial 3-NT formation. These findings strongly support the concept that PN is a crucial player in the secondary damage following SCI. And tempol, by scavenging PN-induced free radicals, provides a promising pharmocotherapeutic strategy for treating acute SCI.

Regular physical activity (PA) leads to an increased quality of life by means of certain physiological adaptations. Regular PA is beneficial to the human body and its functionality, including the physiological, biochemical and even psychological modalities. During PA an increased burden is placed on all physiological mechanisms due to the increased energy demand, resulting in an adaptation of the physiological systems. Currently the biochemical mechanisms by which these adaptations occur are not well understood or defined. During the flow of electrons through the electron transport chain in the mitochondria free radicals and reactive oxygen species (ROS) are produced. PA results in increased ROS production. The relationship of different exercise intensities and ROS production with resulting DNA damage is unclear. These free radicals and ROS disturb the pro-oxidant anti-oxidant balance resulting in oxidative stress. When this balance is disturbed oxidative stress could lead to potential oxidative damage, Oxidative damage occurs in lipid, protein and nucleic acid macromolecules. ROS can attack DNA bases or deoxyribose residues to produce damaged bases and/or single and double strand breaks. When the DNA is regarded and the damages are replicated it could cause mutations or apoptosis, affecting the cell function and physiology. The purpose of this study was to investigate the influence of different aerobic intensities on oxidative DNA damage and repair in middle aged men by means of the Comet assay. Five PA males and five physically inactive males were assigned to an experimental and control group respectively. The subjects did not differ significantly at baseline. The VO2-max of each subject was determined at baseline. Subjects were then randomly assigned to 60, 70, 80 and 90% of individual baseline VO2-max intensities for an acute exercise intervention of 30 minutes on a bicycle ergometer. Blood sampling was done at baseline, post-exercise and 24 hours post-exercise for oxygen radical absorbance capacity (ORAC) and hydroperoxide analysis (dROM). Peripheral blood was obtained for DNA damage testing by means of Comet analysis at baseline, post-exercise, 5, 15, 30 minutes, and also 6, 12, 24, 48 and 72 hours after exercise. The results obtained indicated that subjects who regularly participate in PA had an increased baseline reading of ORAC and dROM values. ORAC levels after each acute exercise session increased, with the highest increase in the control group, with a decrease in the direction of baseline readings 24 hours post exercise. A biphasic damage-repair cycle over the 72 hour period was observed with the Comet analysis. The most damaged cells occur directly after acute exercise. The highest incidence of DNA damage over a 72 hour period was observed at 70% VO2-max, with the least amount of damage after 90% VO2-max. In conclusion the study indicates stress proteins or other kinds of physiological reaction to minimize the damaging effect of oxidative stress, is in place to restore the cell's homeostasis. Thus PA results in the development of oxidative DNA damage. To minimize DNA damage the optimal intensity for acute physical exercise is between 70-80% VO2-max. At higher intensities the release of stress proteins are initiated to buffer the damaging effect of oxidative stress and to restore homeostasis. / Thesis (M.Sc. (Human Movement Science))--North-West University, Potchefstroom Campus, 2007.

Most organisms experience progressive declines in physiological function as they age. A number of studies in a variety of species support a strong link between oxidative damage, age-related functional declines and life span determination. Here, manipulating the expression levels of superoxide dismutase (SOD) isoenzymes SOD1 and SOD2, resulted in altered functional senescence and survival characteristics in Drosophila. Overexpression of cytosolic Sod1 using the yeast GAL4/UAS system conferred a 30-34% increase in mean life span and resulted in an attenuated senescence of odor avoidance behavior in aging flies. Tissue-specific Sod1 overexpression selectively in the nervous system or muscle failed to reproduce these delayed aging phenotypes suggesting that Sod1 overexpression in these tissues alone was not primarily responsible for the aging effects observed. Graded reduction of mitochondrially localized Sod2 expression in a series of Sod2 mutants led to progressive reductions in life span, accelerated age-related functional declines, mitochondrial oxidative damage and neuronal cell death. Tissue-specific Sod2 knock-down using RNA interference revealed that muscle is a key tissue underlying the accelerated age-related functional decline and mortality observed upon loss of SOD2. Sod2 knock-down in the musculature caused a degenerative phenotype consisting of a dramatic reduction in muscle mitochondrial content and ATP levels, elevated cell death and progressive locomotor dysfunction which culminated in early-onset mortality. Collectively, these studies highlight the important role of SOD enzymes in protecting against the impact of oxidative damage on senescence and survival. These findings also lend further support to the oxidative damage hypothesis of aging.

Uma parcela significativa das lesões na molécula do DNA é causada por espécies reativas de oxigênio e a sua produção excessiva e/ou o funcionamento deficiente dos sistemas celulares antioxidantes, que neutralizam a sua ação, é conhecido como estresse oxidativo. Os danos em células normais são prontamente detectados por um sistema de defesa e, em conseqüência, uma rede intrínseca de sinalizações é ativada, sendo que uma das vias resulta na ativação dos mecanismos de reparo do DNA. O reparo por excisão de bases (BER) parece ser a via preferencial de reparo de bases oxidadas, mas existem outras vias de reparo implicadas na reversão do dano oxidativo. A doença de Alzheimer (DA), uma patologia causada particularmente por danos oxidativos, acomete atualmente cerca de 25 milhões de pessoas no mundo, sendo o risco aumentado a partir dos 65 anos de idade. Com isso, a necessidade da identificação de fatores de risco, além de fatores protetores relacionados à DA, tornou-se de grande importância. Por outro lado, há também a necessidade de estudos em nível molecular, que possam fornecer informações sobre os mecanismos que levam ao desenvolvimento da doença. Nesse sentido, foi realizado no presente trabalho, um estudo de expressão gênica transcricional pelo método de microarranjos de DNA, bem como uma análise por PCR em tempo real para uma série de genes envolvidos na resposta ao dano oxidativo no DNA (percepção de danos e reparo do dano), além de outros genes relacionados à doença. Adicionalmente, foram também avaliadas as quebras na fita dupla de DNA causadas por bases oxidadas, em linfócitos de pacientes de Alzheimer (grau moderado) e indivíduos sadios, usando-se métodos de detecção de bases oxidadas (8-oxoGuanina). Entre os vinte genes analisados pelo método de PCR quantitativa em tempo real, apenas a APOE mostrou-se induzida, enquanto 19 genes (ADAM17, APEX1, APP, BACE1, OGG1 ATM, ATR, TREX1, FEN1, FANCG, RAD17, DUSP, ERCC1, ERCC3, ERCC6, HUS1, RAD9, RAD1, PRKDC) foram reprimidos transcricionalmente. Essa repressão verificada para a maior parte dos genes estudados indica que várias vias de sinalização celular ligadas a respostas ao estresse oxidativo, incluindo-se as várias vias de reparo do DNA, podem estar envolvidas na condição DA. Adicionalmente, a análise de expressão gênica por microarranjos de cDNA indicou uma série de 41 genes significativamente modulados (q < 0,06) (dentre eles, NOTCH1, MARK3, PAK, SMC1L1) mas para a maioria destes não há relatos na literatura sobre uma possível relação com DA. Por essa razão, o método de microarranjos de cDNA aponta novas vias que possam estar alteradas em DA, o que constitui uma informação importante. Em conjunto, os dados obtidos no presente estudo fornecem uma contribuição relevante, que futuramente poderão contribuir em termos de intervenção terapêutica. / A great amount of DNA molecule lesions is caused by reactive oxygen species and its synthesis in excess and/or misfunctioning of antioxidant cell systems, which neutralize its effects, is known as oxidative stress. Damage in normal cells is readily detected by a defence system and as consequence, a complex signaling pathway is activated, among them DNA repair mechanisms. The base excision repair (BER) seems to be the primary repair pathway in base oxidative damages, however there are other pathways that are involved in their repair. The Alzheimers disease (AD), a pathology caused particularly by oxidative damages, hits 25 million people worldwide, and its prevalence increases every 5 years beyond age 65. Therefore, there is an emerging need of finding risk factors, as well as protective factors related do AD. By the other hand, it is also necessary molecular studies, which could provide precious information about the mechanisms which lead to the disease development. In the present work, it was made a study about transcriptional gene expression by cDNA microarray, as well as Real Time PCR analysis in a series of genes involved in oxidative DNA damage response (sensing and damage repair), and others associated with the disease. In addition, it were also evaluated DNA strand breaks induced by oxidized bases in lymphocytes from Alzheimers patients (moderate level) and healthy individuals, by oxidized bases (8- oxoguanine) detection methods. Among the twenty genes tested by the quantitative Real Time PCR assay, only APOE was induced, as the remaining 19 (ADAM17, APEX1, APP, BACE1, OGG1 ATM, ATR, TREX1, FEN1, FANCG, RAD17, DUSP, ERCC1, ERCC3, ERCC6, HUS1, RAD9, RAD1, PRKDC) were found repressed. This observed inhibition in most of genes studied shows that many cell signaling pathways associated to oxidative stress response, including DNA repair pathways, may be also involved in the AD pathology. Additionally, the gene expression analysis by cDNA microarrays showed transcriptional alterations in 41 genes (q < 0.06) (among them, NOTCH1, MARK3, PAK and SMC1L1), but for most of them, there are no reports in the literature about their possible relationship with AD, what brought us new important information. Together, all the data obtained in the preset study provide a relevant contribution, which, in the future, may help on new therapeutic designs.

Os extratos obtidos a partir da própolis vermelha brasileira (PVB) têm sido investigados devido às suas amplas atividades biológicas. Recentemente, em nosso grupo de pesquisa, demonstramos a viabilidade da incorporação de um extrato n-hexânico de PVB em nanoemulsões de uso tópico, bem como sua permeação/retenção em pele de orelha suína. No presente estudo, avaliamos as propriedades físico-químicas e reológicas de hidrogéis contendo essas nanoemulsões visando a obtenção de um produto semissólido adequado para aplicação tópica. Em uma primeira fase, foram preparadas nanoemulsões compostas de núcleo oleoso contendo extrato n–hexânico de PVB, miristato de isopropila, lecitina de ovo (NE) e DOTAP (NE/DT), e fase externa aquosa. O polímero gelificante hidroxietilcelulose foi incorporado às formulações após a sua obtenção por emulsificação espontânea (H-NE e H-NE/DT). As formulações apresentaram-se monodispersas com diâmetro médio na faixa de 200-300 nm, confirmado por microscopia eletrônica de transmissão. H-NE apresentou um potencial zeta negativo (-38mV), enquanto o mesmo parâmetro para H-NE/DT foi positivo (+36mV), devido à presença do lipídeo catiônico DOTAP na formulação. O teor de benzofenonas totais, determinado por cromatografia líquida de alta eficiência (CLAE), foi de cerca de 85 mg/g de extrato. Esses parâmetros mantiveram-se constantes durante 90 dias de armazenamento a 4C. As formulações H/NE e H-NE/DT apresentaram um comportamento não-Newtoniano pseudoplástico. Estudos de permeação/retenção das benzofenonas através da pele de orelha suína foram realizados utilizando células de difusão do tipo Franz. A maior retenção das benzofenonas na pele (18,11 μg/cm² após 8h) foi observada para a formulação H-NE/DT, demonstrando o efeito do lipídeo catiônico DOTAP nesse parâmetro. Em uma última etapa, investigou-se a capacidade das formulações de conferirem proteção à pele de orelha suína frente ao dano oxidativo gerado pela sua exposição à luz UVA/UVB. A proteção da pele de orelha suína foi evidenciada pelas técnicas de TBARS, carbonilação de proteínas e grupamentos tióis totais. Os resultados obtidos sugerem que os Hidrogéis contendo extrato de PVB apresentam propriedades físico-químicas e reológicas adequadas para serem utilizadas topicamente para a prevenção do dano oxidativo causado pela exposição à luz UVA/UVB. / Brazilian red propolis (BRP) extracts have been investigated due to their extensive biological activities. Recently, in our research group, we demonstrated the feasibility of incorporating an n-hexane extract of BRP into topical nanoemulsions, as well as the permeation/retention of these compounds in porcine ear skin. In the present study, we evaluated the physicochemical and rheological properties of hydrogels containing these nanoemulsions in order to obtain a semi-solid product suitable for topical application. In a first step, nanoemulsions composed of an oil nucleus containing BRP n-hexane extract, isopropyl myristate, egg lecithin (NE) and DOTAP (NE/DT), and an aqueous external phase were prepared. The hydroxyethylcellulose gelling polymer was incorporated into the formulations after being obtained by spontaneous emulsification (H-NE and H-NE/DT). The formulations were monodisperse exhibiting a mean diameter in the 200-300 nm range, confirmed by transmission electron microscopy. H-NE presented a negative zeta potential (-38mV), while H-NE/DT showed a positive value (+ 36mV) due to the presence of the cationic lipid DOTAP in the formulation. The total benzophenone content, determined by high performance liquid chromatography (HPLC), was about 85 mg/g extract. These parameters were maintained constant for 90 days of storage at 4°C. The formulations H/NE and H-NE/DT presented a non-Newtonian pseudoplastic behavior. Permeation/retention studies of benzophenones through porcine ear skin were performed using Franz type diffusion cells. The highest retention of benzophenones in the skin (18.11 μg/cm² after 8h) was observed for the H-NE/DT formulation, demonstrating the effect of the DOTAP cationic lipid on this parameter. In a last step, the ability of the formulations to confer protection of porcine ear skin against oxidative damage, generated by its exposure to UVA/UVB light, was investigated. The protection was evidenced by the TBARS, carbonylation of proteins, and total thiol groups techniques. The results obtained suggest that the hydrogels containing BRP have adequate physicochemical and rheological properties to be used topically for the prevention of oxidative damage caused by exposure to UVA/UVB light.

Sepsis is a severe life-threatening critical illness that damages multiple physiological systems. After hospital discharge, more than 70% of severe sepsis survivors report profound weakness which significantly impacts quality of life. Such weakness gives rise to new limitations of daily living, which ultimately leads to loss of independence in many patients. Despite wide recognition of this serious issue by clinicians and researchers alike, the mechanisms contributing to chronic skeletal muscle dysfunction after sepsis are not well understood. Lack of progress in this field is largely due to the absence of an appropriate animal model; current models are either too mild to induce muscle weakness or too severe and cause death within a few days. As such, this dissertation work first focused on establishing a clinically-relevant animal model of sepsis which yields surviving mice with chronic skeletal muscle weakness (Aim 1). This aim involved refining the cecal slurry injection model of polymicrobial sepsis in young adult animals, as well as optimizing the timing, duration, and dose of multiple therapeutic agents. The resulting resuscitation protocol was adapted for use in late-middle-aged animals, and muscle strength was evaluated using an ex vivo system which confirmed significant muscle weakness in sepsis survivors, long after sepsis was resolved. Next, using this novel model, we sought to characterize sepsis-induced long-term muscle dysfunction at the molecular level (Aim 2). The first set of experiments under this aim was designed to identify the primary global mechanism(s) (i.e. atrophy, polyneuropathy, and/or myopathy) responsible for muscle weakness in sepsis survivors. Analysis of the force-frequency curves and specific force measurements led to the conclusion that myopathy is the primary cause. Electron micrograph observation, functional assays, and protein analysis then showed that sepsis survivors’ skeletal muscles are characterized by profound mitochondrial abnormalities and oxidative damage. Collectively, these studies demonstrate that long-term muscle weakness is apparent in sepsis-surviving animals, and the functional decline is associated with unresolved mitochondrial damage and dysfunction. This work suggests that medical treatments beyond targeting muscle wasting alone could allow sepsis survivors to regain function and return to productive lives.

Thesis (M.Sc. (Human Movement Science))--North-West University, Potchefstroom Campus, 2007.

DNA sequences containing contiguous AA or TT mismatches, as well as sequences containing a 3-deazacytidine analogue were synthesized. Irradiation of anthraquinone abstracts an electron from the DNA. The loss of an electron from double-stranded DNA results in the formation of a radical cation that migrates through the DNA where it reacts irreversibly with H2O or O2 at GG steps. Subsequent treatment with piperidine or Fpg enzyme cleaves the backbone of the DNA at the site of reaction. DNA oligomers were designed to contain contiguous AA, TT, or G3-deazacytidine mismatches. It was revealed that the mismatches destabilize the duplex DNA; however, there is no measurable effect on the overall secondary structure of the DNA. The contiguous (AA)n mismatch, where n lt 7, was shown to have no effect on charge migration efficiency. In contrast, the contiguous (TT)n mismatch, where n gt 2, was shown to have near complete inhibition of charge migration through the mismatch region. Charge migration through the G3-deazacytidine mismatch was shown to have no effect on charge migration efficiency as well. Interestingly, reaction at the (G3-deazacytidine)2 base pairs revealed a change in the ratio of oxidative damage at the Gs. In (GC)2 base pairs, the ratio of damage at the two Gs is 10:1 with the majority of damage occurring at the 5-G. However, the (G3-deazacytidine)2 base pairs had an equal distribution of damage at the 5 and 3-Gs, with the amount of total reactivity equaling the (GC)2 base pairs. These findings indicate that the base composition in mismatched DNA determines the effect on charge migration efficiency and trapping reactivity.

Regular physical activity (PA) leads to an increased quality of life by means of certain physiological adaptations. Regular PA is beneficial to the human body and its functionality, including the physiological, biochemical and even psychological modalities. During PA an increased burden is placed on all physiological mechanisms due to the increased energy demand, resulting in an adaptation of the physiological systems. Currently the biochemical mechanisms by which these adaptations occur are not well understood or defined. During the flow of electrons through the electron transport chain in the mitochondria free radicals and reactive oxygen species (ROS) are produced. PA results in increased ROS production. The relationship of different exercise intensities and ROS production with resulting DNA damage is unclear. These free radicals and ROS disturb the pro-oxidant anti-oxidant balance resulting in oxidative stress. When this balance is disturbed oxidative stress could lead to potential oxidative damage, Oxidative damage occurs in lipid, protein and nucleic acid macromolecules. ROS can attack DNA bases or deoxyribose residues to produce damaged bases and/or single and double strand breaks. When the DNA is regarded and the damages are replicated it could cause mutations or apoptosis, affecting the cell function and physiology. The purpose of this study was to investigate the influence of different aerobic intensities on oxidative DNA damage and repair in middle aged men by means of the Comet assay. Five PA males and five physically inactive males were assigned to an experimental and control group respectively. The subjects did not differ significantly at baseline. The VO2-max of each subject was determined at baseline. Subjects were then randomly assigned to 60, 70, 80 and 90% of individual baseline VO2-max intensities for an acute exercise intervention of 30 minutes on a bicycle ergometer. Blood sampling was done at baseline, post-exercise and 24 hours post-exercise for oxygen radical absorbance capacity (ORAC) and hydroperoxide analysis (dROM). Peripheral blood was obtained for DNA damage testing by means of Comet analysis at baseline, post-exercise, 5, 15, 30 minutes, and also 6, 12, 24, 48 and 72 hours after exercise. The results obtained indicated that subjects who regularly participate in PA had an increased baseline reading of ORAC and dROM values. ORAC levels after each acute exercise session increased, with the highest increase in the control group, with a decrease in the direction of baseline readings 24 hours post exercise. A biphasic damage-repair cycle over the 72 hour period was observed with the Comet analysis. The most damaged cells occur directly after acute exercise. The highest incidence of DNA damage over a 72 hour period was observed at 70% VO2-max, with the least amount of damage after 90% VO2-max. In conclusion the study indicates stress proteins or other kinds of physiological reaction to minimize the damaging effect of oxidative stress, is in place to restore the cell's homeostasis. Thus PA results in the development of oxidative DNA damage. To minimize DNA damage the optimal intensity for acute physical exercise is between 70-80% VO2-max. At higher intensities the release of stress proteins are initiated to buffer the damaging effect of oxidative stress and to restore homeostasis. / Thesis (M.Sc. (Human Movement Science))--North-West University, Potchefstroom Campus, 2007.

Os extratos obtidos a partir da própolis vermelha brasileira (PVB) têm sido investigados devido às suas amplas atividades biológicas. Recentemente, em nosso grupo de pesquisa, demonstramos a viabilidade da incorporação de um extrato n-hexânico de PVB em nanoemulsões de uso tópico, bem como sua permeação/retenção em pele de orelha suína. No presente estudo, avaliamos as propriedades físico-químicas e reológicas de hidrogéis contendo essas nanoemulsões visando a obtenção de um produto semissólido adequado para aplicação tópica. Em uma primeira fase, foram preparadas nanoemulsões compostas de núcleo oleoso contendo extrato n–hexânico de PVB, miristato de isopropila, lecitina de ovo (NE) e DOTAP (NE/DT), e fase externa aquosa. O polímero gelificante hidroxietilcelulose foi incorporado às formulações após a sua obtenção por emulsificação espontânea (H-NE e H-NE/DT). As formulações apresentaram-se monodispersas com diâmetro médio na faixa de 200-300 nm, confirmado por microscopia eletrônica de transmissão. H-NE apresentou um potencial zeta negativo (-38mV), enquanto o mesmo parâmetro para H-NE/DT foi positivo (+36mV), devido à presença do lipídeo catiônico DOTAP na formulação. O teor de benzofenonas totais, determinado por cromatografia líquida de alta eficiência (CLAE), foi de cerca de 85 mg/g de extrato. Esses parâmetros mantiveram-se constantes durante 90 dias de armazenamento a 4C. As formulações H/NE e H-NE/DT apresentaram um comportamento não-Newtoniano pseudoplástico. Estudos de permeação/retenção das benzofenonas através da pele de orelha suína foram realizados utilizando células de difusão do tipo Franz. A maior retenção das benzofenonas na pele (18,11 μg/cm² após 8h) foi observada para a formulação H-NE/DT, demonstrando o efeito do lipídeo catiônico DOTAP nesse parâmetro. Em uma última etapa, investigou-se a capacidade das formulações de conferirem proteção à pele de orelha suína frente ao dano oxidativo gerado pela sua exposição à luz UVA/UVB. A proteção da pele de orelha suína foi evidenciada pelas técnicas de TBARS, carbonilação de proteínas e grupamentos tióis totais. Os resultados obtidos sugerem que os Hidrogéis contendo extrato de PVB apresentam propriedades físico-químicas e reológicas adequadas para serem utilizadas topicamente para a prevenção do dano oxidativo causado pela exposição à luz UVA/UVB. / Brazilian red propolis (BRP) extracts have been investigated due to their extensive biological activities. Recently, in our research group, we demonstrated the feasibility of incorporating an n-hexane extract of BRP into topical nanoemulsions, as well as the permeation/retention of these compounds in porcine ear skin. In the present study, we evaluated the physicochemical and rheological properties of hydrogels containing these nanoemulsions in order to obtain a semi-solid product suitable for topical application. In a first step, nanoemulsions composed of an oil nucleus containing BRP n-hexane extract, isopropyl myristate, egg lecithin (NE) and DOTAP (NE/DT), and an aqueous external phase were prepared. The hydroxyethylcellulose gelling polymer was incorporated into the formulations after being obtained by spontaneous emulsification (H-NE and H-NE/DT). The formulations were monodisperse exhibiting a mean diameter in the 200-300 nm range, confirmed by transmission electron microscopy. H-NE presented a negative zeta potential (-38mV), while H-NE/DT showed a positive value (+ 36mV) due to the presence of the cationic lipid DOTAP in the formulation. The total benzophenone content, determined by high performance liquid chromatography (HPLC), was about 85 mg/g extract. These parameters were maintained constant for 90 days of storage at 4°C. The formulations H/NE and H-NE/DT presented a non-Newtonian pseudoplastic behavior. Permeation/retention studies of benzophenones through porcine ear skin were performed using Franz type diffusion cells. The highest retention of benzophenones in the skin (18.11 μg/cm² after 8h) was observed for the H-NE/DT formulation, demonstrating the effect of the DOTAP cationic lipid on this parameter. In a last step, the ability of the formulations to confer protection of porcine ear skin against oxidative damage, generated by its exposure to UVA/UVB light, was investigated. The protection was evidenced by the TBARS, carbonylation of proteins, and total thiol groups techniques. The results obtained suggest that the hydrogels containing BRP have adequate physicochemical and rheological properties to be used topically for the prevention of oxidative damage caused by exposure to UVA/UVB light.