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ORAL PRESENTATION / TAM METİN SÖZLÜ SUNUM

cells (Liu et al., 2016). The primary ways doxorubicin leads to cardiotoxicity is inflammation
and apoptosis (El-Refaiy et al., 2025).

In recent years, extensive research has been conducted to investigate the effects of
various phytochemical compounds. A promising approach to mitigate cardiotoxicity is the

use of phytochemicals, which are plant-derived small molecules with antioxidant, anti-

inflammatory, and anti-apoptotic properties. These natural agents have shown considerable
therapeutic potential in the management of cardiovascular diseases. A wide range of

phytoconstituents have been investigated, with accumulating data supporting their efficacy
in attenuating cardiotoxicity (Birdal et al., 2024). Moreover herbal extracts—administered

either alone or in combination with conventional chemotherapeutic agents, have been
reported to alleviate inflammation and cellular injury induced by xenobiotics or synthetic

drugs such as doxorubicin (El-Refaiy et al., 2025).

Blueberry seed oil is a valuable component utilized in the nutraceutical, food, and
cosmetic industries. Its richness in essential polyunsaturated fatty acids offers significant

potential health benefits to consumers. The fatty acid composition includes palmitic (C16:0),
stearic (C18:0), oleic (C18:1), linoleic (C18:2n-6), and α-linolenic (C18:3n-3, ALA) acids.

These constituents contribute to the oil’s antioxidant properties. In particular, α-linolenic acid
is an essential omega-3 fatty acid that cannot be synthesized by the human body and must

be obtained through diet. ALA has been reported to reduce the risk of cardiovascular
diseases, cancer, hypertension, and autoimmune disorders. Furthermore, a low n-6/n-3 ratio

is considered an important advantage for cardiovascular health. Therefore, blueberry seed
oil, with its high α-linolenic acid content and balanced fatty acid profile, represents a

functional oil source with the potential to support cardiovascular health (Li et al., 2016; Parry

et al., 2005).
Cardiac tissue response to toxic compounds is mediated by two interrelated pathways.

The activation of nuclear factor-κB (NF-κB) induces the transcription of proinflammatory
cytokines, particularly tumor necrosis factor alpha (TNF-α), thereby driving inflammatory

responses. Moreover, xenobiotic-induced signaling promotes caspase activation, with
caspase-3 serving as a key executioner of the apoptotic cascade. Collectively, xenobiotic-

induced NF-κB and TNF-α signaling in cardiomyocytes may lead to inflammation, whereas
caspase-3 activation triggers apoptosis, thereby contributing to cardiotoxic effects (Luo et

al., 2019; Zha et al., 2023).

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