Protective Effects of Diets Rich in Polyphenols in Cigarette Smoke (CS)-Induced Oxidative Damages and Associated Health Implications

Abstract

Cigarette smoking has been responsible for causing many life-threatening diseases such as pulmonary and cardiovascular diseases as well as lung cancer. One of the prominent health implications of cigarette smoking is the oxidative damage of cellular constituents, including proteins, lipids, and DNA. The oxidative damage is caused by reactive oxygen species (ROS, oxidants) present in the aqueous extract of cigarette smoke (CS). In recent years, there has been considerable interest in the potential health benefits of dietary polyphenols as natural antioxidant molecules. Epidemiological studies strongly suggest that long-term consumption of diets (fruits, vegetables, tea, and coffee) rich in polyphenols offer protective effects against the development of cancer, cardiovascular diseases, diabetes, osteoporosis, and neurodegenerative diseases. For instance, green tea has chemopreventive effects against CI-induced lung cancer. Tea might prevent CS-induced oxidative damages in diseases because tea polyphenols, such as catechin, EGCG, etc., have strong antioxidant properties. Moreover, apple polyphenols, including catechin and quercetin, provide protection against CS-induced acute lung injury such as chronic obstructive pulmonary disease (COPD). In CS-induced health problems, the antioxidant action is often accompanied by the anti-inflammatory effect of polyphenols. In this narrative review, the CS-induced oxidative damages and the associated health implications/pathological conditions (or diseases) and the role of diets rich in polyphenols and/or dietary polyphenolic compounds against various serious/chronic conditions of human health have been delineated.

A Signaling Crosstalk Links SNAIL to the 37/67 kDa Laminin-1 Receptor Ribosomal Protein SA and Regulates the Acquisition of a Cancer Stem Cell Molecular Signature in U87 Glioblastoma Neurospheres

“…Thus, understanding the impact of diet-derived molecules on the early signaling events that would prevent oncogenic transformation of normal stem cells could halt the emergence of CSC, although these can also originate from de-differentiation of bulk tumor cells. Diet-derived phenolic compounds could represent such a vast group of chemopreventive substances against the emergence of CSC with anticarcinogenic functions, anti-inflammatory, and antioxidative activities [ 33 ].…”

Potential Role of Natural Antioxidant Products in Oncological Diseases

“…Epidemiological and experimental evidence suggests that polyphenols may act as chemopreventive agents that delay, suppress, or reverse cancer progression to advanced lung cancer through various mechanisms. These include antioxidant/anti-inflammatory activities, modulation of biotransformation enzymes, antiproliferative effect, and immune system modulation [ 110 , 111 ]. A meta-analysis of eight prospective and seven case-control studies showed that isoflavone intake was significantly associated with decreased risk of lung cancer (RR 0.91, 95% CI: 0.84, 0.87) [ 107 ].…”

β-Caryophyllene Counteracts Chemoresistance Induced by Cigarette Smoke in Triple-Negative Breast Cancer MDA-MB-468 Cells

“…In this context, along with early diagnosis, a great interest has been devoted towards chemopreventive agents, which can be exploited by both healthy and oncological subjects to prevent or repair CS damage, thus limiting the occurrence and aggressiveness of breast cancers. Preclinical studies highlighted the possible benefits of anti-inflammatory drugs, dietary polyphenols and other natural compounds against the oxidative and inflammatory damage by cigarette smoke, however limited evidence about their ability to hinder cancer progression and chemoresistance development is currently available [ 26 , 114 , 115 , 116 , 117 , 118 , 119 ], and the true mechanisms involved remain to be elucidated. In this context, our results provide additional evidence about the mechanisms implicated in the chemoresistance induced by cigarette smoke in triple-negative breast cancer cells, particularly the increased proliferative abilities, probably due to a lowered control in G2/M phase, the promotion of autophagic cell death and migration, along with the STAT3 activation, which seem to be activated as buffering processes to promote the cancer cell resilience to the acute CSC damage, thus resulting in the increased recovery abilities.…”