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Plasma membrane integrity and oxidative stress index outcomes of canine progenitor epidermal keratinocytes ( CPEK s) exposed to virgin coconut oil ( VCO )
Author(s) -
Boyd Megan,
Morris Jordan M.,
Santoro Domenico
Publication year - 2019
Publication title -
veterinary dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.744
H-Index - 60
eISSN - 1365-3164
pISSN - 0959-4493
DOI - 10.1111/vde.12800
Subject(s) - nitrite , lactate dehydrogenase , oxidative stress , andrology , chemistry , griess test , microbiology and biotechnology , biochemistry , medicine , biology , enzyme , organic chemistry , nitrate
Background There is a rapidly growing market for topical use of virgin coconut oil ( VCO ). Studies of topical use in dogs are lacking. Hypothesis/Objective The objective of this study was to measure the release of lactate dehydrogenase ( LDH , a plasma membrane disruption marker) and production of nitrite (Griess reaction, an oxidative stress marker) from a canine keratinocyte cell line after exposure to VCO as an initial toxicity screening to suggest future studies. Methods and materials Canine progenitor epidermal keratinocytes ( CPEK s) were plated onto permeable transwell membranes and cultured with undiluted organic VCO or control media. Following a 24 h incubation, an LDH assay and a Griess reaction were performed on the collected subnatants. Results Exposure of CPEK s to VCO significantly increased LDH release compared to controls, 62.29 ± 16.32% versus 8.88 ± 5.82% ( P = 0.0056) and there was no significant difference in production of nitrite compared to controls, 2.47 ± 1.56 μmol/L versus 1.42 ± 0.95 μmol/L ( P = 0.086). Conclusions and clinical importance Based on this study VCO induced an increased disruption of plasma membrane integrity, as measured by LDH . However, VCO did not induce increased oxidative stress, as measured by nitrite production. Based on these preliminary data, further studies to assess the toxicity of VCO are needed.