In recent years, the safety of sunscreens to coral reefs and the role these products would play in the process of coral bleaching has been a concern. However, the discussion centers almost exclusively on the organic components used as UV filters, with little attention given to inorganic UV filters, such as zinc oxide. Zinc oxide nanoparticles (ZnO-NPs) have been a common ingredient of sunscreen formulations for decades and are being discharged in coral reef environments. Even though there are data supporting that ZnO is toxic to certain species of fish and algae, regulatory agencies do not appear concerned with the possible outcome of the exposure of corals and their algal symbionts to this metal oxide. This review compiles the published work on the toxicity of ZnO and ZnO-NPs to corals and zooxanthellae, which strongly supports the notion that zinc oxide is toxic to both corals and microalgae. In view of this, concern has been raised by the use of the “reef safe” label to promote sunscreens that lack specific organic components, however containing ZnO as the major UV filter. years However filters ZnONPs NPs (ZnO-NPs environments algae zooxanthellae microalgae safe filter

Fitato (PHYT, mio-inositol 1,2,3,4,5,6-hexakisfosfato) é um produto natural com forte efeito sobre a biodisponibilidade de minerais, especialmente o ferro. Neste trabalho, investigamos os efeitos antioxidantes do PHYT em modelos de transtornos de sobrecarga de ferro (ferro lábil plasmático e reservatório de ferro lábil). PHYT apresentou um efeito antioxidante considerável, com a vantagem de ser permeável às células e ser um constituinte normal da dieta humana. Nossos resultados sugerem que o PHYT pode auxiliar as defesas do organismo contra estresse induzido por sobrecarga de ferro.

Phytate (PHYT, myo-inositol 1,2,3,4,5,6-hexakisphosphate) is a natural product with strong effect on the bioavailability of minerals, especially iron. In this work, we investigated the antioxidant effects of PHYT on models of iron overload disorders (labile plasma iron and labile iron pool) both in solution and in HeLa cells. PHYT has a considerable antioxidant effect, with the benefit of being cell permeant and a normal constituent of human diet. Our results suggest that PHYT may assist organism defenses against iron-overload stress.

O efeito do ácido S,S-etilenodiaminodi-succínico (edds) na supressão da oxidação do ácido ascórbico catalisada por metais (Mn, Fe, Co, Ni, Cu, Zn) foi testado in vitro através da oxidação da sonda fluorescente cloreto de 1,2,3-diidrorodamina. A atividade pró-oxidante do ferro não foi totalmente suprimida, mesmo sob excesso molar de quatro vezes do ligante. O efeito do meio de cultura na toxicidade dos complexos para células mononucleares do sangue periférico (PBMC) e da linhagem K562 foi estudado. A citotoxicidade de Fe-edds foi abolida na presença de Trolox ou de proteínas do soro. Os prováveis mecanismos de toxicidade celular foram investigados através do bloqueio de transportadores de monocarboxilatos (MCT) e estudos de ciclo celular por citometria de fluxo. Células tratadas com os complexos metálicos e com o ácido alfa-ciano-4-hidroxicinâmico, um conhecido bloqueador de MCT, mostraram recuperação de viabilidade, sugerindo que esses transportadores possam estar envolvidos na internalização dos complexos metal-edds. O ácido livre promoveu a parada do ciclo celular na fase G0/G1 (PBMC) ou S (K562), sugerindo dano direto ao DNA ou interferência na sua duplicação.

The effect of S,S-ethylenediaminedisuccinic acid (edds) on the quenching of metal-catalyzed (metal = Mn, Fe, Co, Ni, Cu, Zn) oxidation of ascorbic acid was tested in vitro via oxidation of the fluorescent probe 1,2,3-dihydrorhodamine dihydrochloride. The pro-oxidant activity of iron was not fully suppressed, even at a four-fold molar excess of the ligand. The effect of serum on the toxicity to peripheral blood mononuclear cells (PBMC) and K562 cells was investigated. The cytotoxic effect of Fe-edds was abrogated in the presence of Trolox or serum proteins. The probable pathways of cell toxicity were investigated through blocking of the monocarboxylate transporters (MCT) in association with cell cycle studies by flow cytometry. Cells treated with metal complexes and alpha-cyano-4-hydroxycinnamic acid, a known MCT inhibitor, showed recovery of viability, suggesting that MCT proteins may be involved in the internalization of metal-edds complexes. The free acid induced cell cycle arrest in G0/G1 (PBMC) and S (K562) phases, suggesting direct DNA damage or interference in DNA replication.

Cinco complexos de ródio(II) de fórmula geral [Rh2(ponte)4] (ponte = acetato, propionato, butirato, trifluoroacetato e trifluoroacetamidato) tiveram suas afinidades em relação à albumina humana (HSA) determinadas por espectrofotometria, observando-se no caso dos alquilcarboxilatos uma correlação inversa com suas lipossolubilidades. A difusão dos complexos livres ou ligados à proteína para células de Ehrlich in vitro parece primordialmente governada pelo caráter hidrofóbico do complexo. O complexo [Rh2(tfc)4] apresentou afinidade pela proteína (K = 214,1), além de partição celular tanto em ausência (32,1%) como na presença (48,6%) de HSA. Desta forma, o composto HSA: [Rh2(tfc)4] teve sua ação antitumoral investigada em camundongos Balb-c portadores de ascite de Ehrlich, mostrando que a HSA pode ser um reservatório para o complexo de ródio.

The affinities for human albumin (HSA) of five rhodium(II) complexes of general formula [Rh2(bridge)4] (bridge = acetate, propionate, butyrate, trifluoroacetate and trifluoroacetamidate) were determined by spectrophotometry. In the case of the alkylcarboxylates, an inverse correlation of affinity with their liposolubilities was observed. Diffusion of the free or protein-bound complexes into Ehrlich cells in vitro seems to be primarily governed by the hydrophobic character of the complex. The complex [Rh2(tfc)4] exhibited affinity towards the protein (K = 214.1) as well as cell partition both in the absence (32.1%) and presence (48.6%) of HSA. The compound HSA: [Rh2(tfc)4] has had its antitumoral action in tumor-bearing Balb-c mice investigated, showing that HSA can be a drug reservoir for the rhodium complex.