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The object of this study was to evaluate the relationship between oxidative damage induced by oxaliplatin (OXA) and the therapeutic potential of 7-chloro-4-(phenylselanyl) quinoline (4-PSQ) in kidney of mice. Mice received OXA (10 mg/kg) or vehicle intraperitoneally (days 0 and 2). Oral administration of 4-PSQ (1 mg/kg) or vehicle was performed on days 2 to 14. On day 15 the animals were euthanized and the kidneys and blood were collected. The effect of OXA and (or) 4-PSQ on urea, thiobarbituric acid reactive species, nonprotein thiol (NPSH), and protein carbonyl (PC) levels were investigated. Moreover, renal superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), S-aminolevulinic acid dehydratase ([delta] -ALA-D), and [Na.sup.+], [K.sup.+] ATPase activities were evaluated. Our findings revealed an increase on urea levels and significant renal oxidative damage in OXA-induced mice. OXA exposure increased SOD, GPx, and GST activities and caused a reduction on NPSH levels and CAT and GR activities. [Na.sup.+], [K.sup.+] ATPase and [delta]-ALA-D activities were reduced by OXA. 4-PSQ decreased plasmatic urea levels and renal oxidative damage. SOD, GPx, CAT, GR, and [Na.sup.+], [K.sup.+] ATPase activities were restored by 4-PSQ.4-PSQ may be a good prototype for the treatment of OXA-induced renal injury. Keywords: oxaliplatin, selenium, nephroprotection, quinoline, oxidative stress. Cette etude avait pour but d'evaluer le lien entre les dommages oxydatifs entraines par l'oxaliplatine (OXA) et le potentiel therapeutique de la 7-chloro-4-(phenylselanyl) quinoline (4-PSQ) dans le rein chez la souris. Les souris ont recu de l'OXA (a 10 mg/kg) ou le vehicule par voie intraperitoneale aux jours 0 et 2. Nous avons procede a l'administration orale de 4-PSQ (1 mg/kg) ou du vehicule aux jours 2 a 14. Au jour 15, nous avons euthanasie les animaux et preleve les reins et du sang. Nous avons etudie l'effet de l'OXA et/ou de la 4-PSQ sur les taux de produits reactifs de l'acide thiobarbiturique, des thiols non proteiques (NPSH) et du carbonyl proteique (PC). En outre, nous avons evalue l'activite de la superoxyde dismutase (SOD), de la catalase (CAT), de la glutathion peroxydase (GPx), de la glutathion reductase (GR), de la glutathion S- transferase (GST), de la deshydratase de l'acide [delta]-aminolevulinique ([delta]-ALA-D) et de la [Na.sup.+]/[K.sup.+] ATPase. Nos resultats ont revele une augmentation des taux d'uree, et des dommages oxydatifs importants dans les reins des souris OXA. L'exposition a l'OXA entrainait une hausse de l'activite de la SOD, de la GPx et de la GST, ainsi qu'un abaissement des taux de NPSH de meme que de l'activite de la CAT et de la GR. L'OXA entrainait un abaissement de l'activite de la [Na.sup.+]/[K.sup.+] ATPase et de l'[delta]-ALA-D. Mais la 4-PSQ entrainait une diminution des taux d'uree plasmatique et des dommages oxydatifs renaux. De fait, l'activite de la SOD, de la GPx, de la CAT, de la GR et de la [Na.sup.+]/[K.sup.+] ATPase se retablissait avec la 4-PSQ. En conclusion, la 4-PSQ pourrait constituer un bon prototype pour le traitement des lesions renales entrainees par l'OXA. [Traduit par la Redaction] Mots-cles: oxaliplatine, selenium, nephroprotection, quinoline, stress oxydatif., 1. Introduction According to American Cancer Society, Surveillance and Health Services Research (Miller et al. 2016), chemotherapy treatment is used by 56% of patients with cancer; however, toxicity is a [...]

There is an increasing incidence of hepatotoxicity induced by oxaliplatin (OXA); therefore, researchers' attention has been drawn to therapeutic alternatives that may decrease OXA-induced hepatotoxicity. Studies indicate that oxidative stress plays a major role in OXA-induced liver injury. As several pharmacological effects of 7-chloro-4-(phenylselanyl) quinole (4-PSQ) involve its antioxidant action, the hypothesis that this organoselenium compound could be promising for the treatment or prevention of hepatotoxicity induced by treatment with OXA was investigated. To test this hypothesis, male Swiss mice received OXA (10 mg * [kg.sup.-1]) on days 0 and 2, followed by oral administration of 4-PSQ (1 mg * [kg.sup.-1]) on days 2 to 14. 4-PSQ reduced the plasma aspartate, and alanine aminotransferase activity increased by exposure to OXA. The histopathological examination of the liver showed that 4-PSQ markedly improved OXA-induced hepatic injury. In addition, treatment with 4-PSQ reduced the oxidation of lipids and proteins (thiobarbituric acid reactive species levels and protein carbonyl content) and attenuated the increase of hepatic catalase and glutathione peroxidase activity caused by OXA. The inhibition of hepatic [delta]-aminolevulinic dehydratase activity induced by OXA was reverted by 4-PSQ. In conclusion, results indicate that 4-PSQ may be a good therapeutic strategy for attenuating OXA-induced liver damage. Key words: oxaliplatin, colorectal cancer, hepatotoxicity, oxidative stress, selenium, quinoline, antioxidant. On remarque une augmentation de la frequence de l'hepatotoxicite engendree par l'oxaliplatine (OXA). Par consequent, l'attention des chercheurs s'est tournee vers d'autres choix therapeutiques qui pourraient entrainer une diminution de l'hepatotoxicite engendree par l'OXA. Les etudes montrent que le stress oxydatif joue un role majeur dans les lesions hepatiques provoquees par l'OXA. Puisque plusieurs effets pharmacologiques de la 7-chloro-4-(phenylselanyl) quinole (4-PSQ) passent par son effet antioxydant, nous avons mis a l'epreuve l'hypothese selon laquelle ce compose d'organoselenium peut etre prometteur pour la prevention ou le traitement de l'hepatotoxicite engendree par l'administration d'OXA. Nous nous y sommes appliques a l'aide de souris suisses auxquelles etait administre de l'OXA (a 10 mg * [kg.sup.-1]) aux jours 0 et 2, avec ensuite l'administration de 4-PSQ a raison de 1 mg * [kg.sup.-1] par voie orale aux jours 2 a 14. La 4-PSQ entrainait une diminution de l'activite plasmatique de l'aspartate et de l'alanine aminotransferase accrue par l'exposition a l'OXA. L'examen histopathologique du foie a montre que la 4-PSQ permettait d'attenuer de facon marquee les lesions hepatiques engendrees par l'OXA. De plus, l'administration de 4-PSQ entrainait une diminution de l'oxydation des lipides et des proteines (taux de derives reactifs de l'acide thiobarbiturique et de proteines couplees a un groupement carbonyle), avec une attenuation de l'augmentation de l'activite de la catalase et de la glutathion peroxydase hepatiques entrainee par l'OXA. La 4-PSQ entrainait une inversion de l'inhibition de l'activite de la deshydratase [delta]-aminolevulinique hepatique engendree par l'OXA. En conclusion, les resultats montrent que l'administration de 4-PSQ pourrait constituer une bonne strategie en vue d'attenuer les dommages hepatiques engendres par l'OXA. [Traduit par la Redaction] Mots-cles : oxaliplatine, cancer colorectal, hepatotoxicite, stress oxydatif, selenium, quinoline, antioxydant., Introduction Cancer is the second leading cause of death worldwide (Fitzmaurice et al. 2017). An incidence of 18 million new cancer cases and 9 million deaths from cancer was estimated [...]

Given that particle and bubble size, as well as their surface properties, are pivotal in froth flotation, surfactants have been extensively employed due to their impact on bubble size and froth stabilization. This study aimed to investigate the influence of surfactants on the performance of apatite flotation in column. Three different categories of surfactants were examined: anionic, amphoteric, and nonionic, specifically Lupromin, Genagen, and Triton X-100, respectively. The critical coalescence concentration (CCC) and surface tension of each surfactant were determined. The impact of these surfactants on reducing bubble size was quantified, and their subsequent effects on apatite flotation in a column were assessed. The most favorable flotation response for Genagen was achieved at CCC and pH 11, resulting in the highest apatite recovery and the smallest bubble size. For Triton X-100, the best condition was attained at ¼ CCC and pH 11. However, overall, Lupromin was the surfactant that yielded the best flotation results (at ¼ CCC and pH 11). The superior performance of this anionic surfactant was corroborated by chemical adsorption results, as demonstrated by FTIR analyses. [ABSTRACT FROM AUTHOR]

The main mechanism of flotation is bubble-particle interaction, which is strongly dependent on the particle size and the bubble size distribution (BSD). It is known that air bubbles are responsible for collecting and delivering hydrophobic particles from the pulp to the foam zone. Controlling the size and distribution of bubbles generated is essential to promote greater bubble-particle interaction. The aim of this study was to investigate the influence of bubble size on the flotation performance of apatite of a low-grade phosphate ore for different particle sizes: fine (d32 = 13.95 µm), intermediate (d32 = 50.86 µm), and coarse (d32 = 108.96 µm). Through the results, it was possible to identify the best bubble size range for each particle size studied. The fine particles showed a better flotation performance when medium-sized bubbles (800–1,000 µm) were used, while the coarse particles had an improved performance when large bubbles (d32 > 1,000 µm) were used. However, the best flotation result was obtained with intermediate particles, which accepted a large range of bubble size distribution under different operating conditions since the collision and attachment mechanisms are favored in this particle size range. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate whether (E)-2-benzylidene-4-phenyl-1, 3-diselenole (BPD) protects against hepatotoxicity induced by thioacetamide (TAA). On the first day of treatment, male adult Wistar rats received BPD (10 or 50 mg x [kg.sup.-1]). On the second day, the rats received a single intraperitoneal injection of TAA (400 mg x [kg.sup.-1]). Twenty-four hours after TAA administration, biochemical determinations and liver histological analysis were carried out. BPD (50 mg x [kg.sup.-1]) reduced plasma aspartate and alanine aminotransferase, alkaline phosphatase, and lactate dehydrogenase activities increased by TAA exposure. Treatment with BPD was effective against increased lipid peroxidation levels and attenuated a decrease in hepatic reduced glutathione and ascorbic acid levels as well as an inhibition of glutathione peroxidase activity caused by TAA exposure. The higher dose of BPD protected against the inhibition of hepatic [delta]-aminolevulinic dehydratase activity induced by TAA. Finally, histopathological examination of the liver showed that BPD markedly ameliorated TAA-induced hepatic injury. In conclusion, BPD protected against hepatotoxicity and oxidative stress caused by TAA exposure in rats. Key words: selenium, thioacetamide, oxidative stress, liver, antioxidant. Ces travaux avaient pour but d'etudier si le (E)-2-benzylidene-4-phenyl-1, 3-diselenole (BPD) assure une protection contre l'hepatotoxicite provoquee par le thioacetamide (TAA). Des rats Wistar males adultes ont recu du BPD (10 ou 50 mg x [kg.sup.-1]) le premier jour du traitement. Le deuxieme jour, les rats ont recu une injection intraperitoneale unique de TAA (400 mg x [kg.sup.-1]). Nous avons procede a des analyses biochimiques et a l'examen histologique du foie 24 heures apres l'administration de TAA. Le BPD (50 mg x [kg.sup.-1]) permettait d'attenuer les augmentations de l'activite de l'aspartate et de l'alanine aminotransferase, de la phosphatase alcaline et de la deshydrogenase lactique causees par l'exposition au TAA. Le traitement par le BPD etait efficace contre l'augmentation des taux de peroxydation lipidique et attenuait la diminution des taux de glutathion reduit et d'acide ascorbique ainsi que l'inhibition de l'activite de la glutathion peroxydase causees par l'exposition au TAA. La dose de BPD la plus elevee assurait une protection contre l'inhibition de l'activite de la deshydratase [delta]-aminolevulinique hepatique provoquee par le TAA. Enfin, l'examen histopathologique du foie montrait que le BPD permettait d'attenuer de facon marquee les lesions hepatiques provoquees par le TAA. En conclusion, le BPD assurait une protection contre l'hepatotoxicite et le stress oxydatif causes par l'exposition au TAA chez le rat. [Traduit par la Redaction] Mots-cles: selenium, thioacetamide, stress oxydatif, foie, anti-oxydant., Introduction The liver plays a key role in the metabolism and excretion of xenobiotics. Nevertheless, it is susceptible to damage from a number of drugs and toxins (Lee 2003). Rodent [...]