Content: Different tanning materials endow leather with varying colors observable in undyed leathers. Periodateoxidized starch tanned leathers have a yellow tinge or light brown color and get darker with age. The color change in situ is ascribable to iodate ions that are byproducts of periodate oxidation. Iodate ions undergo reduction to form iodine molecules that are yellow or brown in low or at higher concentrations. This study focuses on the removal of iodate ions from Dialdehyde Tapioca Starch (DTS) using a simple precipitation method. Preparation of DTS is by periodate oxidation and precipitation of iodate ions using an inorganic precipitant. The experiments for manufacturing wet-white leathers used pickled goatskins and DTS (unmodified and modified) tanning agents at various percentages based on pelt weight. Glutaraldehyde (GTA) tanning was the control. The percentage removal of iodate ions in modified DTS was 98%. Both unmodified and modified DTS had an aldehyde content of 70%. FT-IR and 1H-NMR confirmed the aldehyde groups. GTA, unmodified, and modified DTS tanned leathers had shrinkage temperatures of 80, 87, and 89°C, respectively. The physico-mechanical properties of the control and experimental leathers are comparable. GTA tanned leather had the typical brown color associated with GTA tannages. The ‘b’ color value of unmodified DTS tanned leather was high confirming yellowing of leathers upon ageing. Wet-white leather tanned with modified DTS had no discernible color change. Analysis of the spent tan liquor shows a reduction in the BOD, COD, TS, and TDS load when compared to GTA tanning system evincing the biodegradability of DTS. This study has overcome the drawback associated with periodate-oxidized starch tanning agents, viz. leather darkening over time, considering the chemical and physico-mechanical properties of the resultant leathers. The novel iodate free DTS can be scaled-up for commercial availability. Take-Away: Removal of iodate ions from periodate-oxidized starch before its use as a tanning agent is imperative to avoid leather color change over time. This study reports the successful removal of iodate ions from Dialdehyde Tapioca Starch (DTS). Wet-white leather tanned with the modified DTS had no observable color change upon ageing.

L'épithélium pigmentaire rétinien (EPR) est une monocouche formée de cellules hautement spécialisées et uniques dont les nombreuses fonctions servent à maintenir une vision adéquate. En revanche, ces fonctions spécifiques rendent les cellules de l’EPR particulièrement vulnérables au stress oxydant. Avec le vieillissement, les cellules de l’EPR peuvent dégénérer et devenir non-fonctionnelles, donnant lieu à plusieurs maladies telles que la dégénérescence maculaire liée à l'âge (DMLA). Dans les pays occidentaux, la DMLA est la principale cause de cécité et de déficience visuelle chez les personnes âgées. En fait, environ 90 % des patients atteints de la DMLA souffrent de la forme sèche, pour laquelle il n'existe aucun traitement. Des années de recherche ont établi que le stress oxydant est un contributeur majeur à la pathogenèse de la DMLA sèche. De nombreuses études ont montré que le stress oxydant induit les cellules de l’EPR à libérer des vésicules extracellulaires (VEs). Nos propres travaux ont démontré que les VEs peuvent induire le stress oxydant et la sénescence chez les cellules de l’EPR. Comme d'autres, nous avons constaté que les VEs étaient enrichis en microARNs. Grâce au séquençage d’ARN, nous avons identifié le let-7f comme étant l'un des microARNs les plus abondants contenus dans ces vésicules. L'objectif de ce mémoire a été l’exploration entre la relation let-7f et la dégénérescence des cellules de l’EPR. Nos résultats ont démontré une régulation et une augmentation de l’expression du let-7f dans les cellules de l’EPR sous stress oxydant, in vitro et in vivo. De plus, la surexpression du let-7f a généré un stress oxydant, le dysfonctionnement et la sénescence des cellules humaines de l’EPR (ARPE-19). De plus, l’inhibition du let-7f à protéger ces cellules contre les conséquences néfastes induites par l’iodate de sodium. En somme, les résultats de ce travail suggèrent fortement que le let-7f est impliqué dans la dégénérescence des cellules de l’EPR et pourraient aider à la découverte de nouveaux processus pertinents dans la pathogenèse de la DMLA sèche. / The retinal pigment epithelium (RPE) is a highly specialized and unique monolayer of cells whose many functions are vital for maintaining proper vision. In turn, these specific functions render RPE cells particularly vulnerable to oxidative injury. With age, RPE cells can degenerate and become dysfunctional, giving rise to various disorders such as age-related macular degeneration (AMD). In western countries, AMD is the primary cause of blindness and visual impairments in the elderly. In fact, approximately 90% of all AMD patients suffer from the dry form of the disease, for which there exist no approved treatment. Decades of research have established that chronic oxidative stress is a major contributor to the pathogenesis of dry AMD. Numerous studies have shown that oxidative stress induces RPE cells to release extracellular vesicles (EVs) which participate in cell-to-cell communication. Our recent work has demonstrated that EVs alone were sufficient in inducing oxidative stress and senescence in RPE cells. Consistent with others, we found that EVs released by RPE cells were enriched in microRNAs. RNA-sequencing identified let-7f as one of the most abundant miRNAs contained in these vesicles. Despite being one of the first miRNAs to be discovered, the role of let-7f in RPE cells has remained essentially unexplored. The aim of this dissertation was to investigate the relationship between let-7f and RPE cells in regards to their degeneration and dysfunction. Our results revealed that the expression of let-7f increased and was regulated by oxidative stress in RPE cells, in vitro and in vivo. In addition, let-7f overexpression promoted oxidative stress, cellular dysfunction and senescence in human RPE (ARPE-19) cells. Finally, inhibition of let-7f exhibited protective effects against sodium iodate-induced oxidative injury. Overall, the findings in this work provide strong evidence that let-7f is implicated in the degeneration of RPE cells and further mechanistic investigation may help to uncover novel insights into the genesis of dry AMD.