400
Views
20
CrossRef citations to date
0
Altmetric
ORIGINAL RESEARCH

Antioxidant Diet Protects Against Emphysema, but Increases Mortality in Cigarette Smoke-Exposed Mice

, , &
Pages 362-368 | Published online: 11 Aug 2011

Figures & data

FIGURE 1  Antioxidant diet protects against cigarette smoke-induced emphysema, but potentiates CS-induced mortality. (A) Survival. Each group of 15 age-matched C3H mice fed with regular diet (RD) or AOD were exposed to filtered air (FA), a low concentration of CS (TPM 100 mg/m3; LCS) or a high concentration of CS (TPM 250 mg/m3; HCS) and survival was monitored over 16 weeks. Only the numbers of CS-exposed mice are shown because there was no death in filtered air-exposed mice. Survival curves were analyzed by Kaplan-Meier tests, using Bonferroni corrections on the Gehan-Breslow-Wilcoxon P-values. (B) Representative photomicrographs of lungs from surviving mice processed for H & E staining (10 × original magnification). (C) Quantification of emphysema scores. The values in panel C are the mean ± SEM of the emphysema score in the surviving mice in the groups (n = 8 except for 7 mice in the AOD/LCS group, 6 mice in the RD/HCS group, and 3 mice in the AOD/HCS group). The bracketed value is from a pairwise (Mann-Whitney) comparison (*P < 0.05). (D) The whole body weight of the surviving mice in each group was monitored every 2 weeks. Data are expressed as mean ± SEM.

FIGURE 1  Antioxidant diet protects against cigarette smoke-induced emphysema, but potentiates CS-induced mortality. (A) Survival. Each group of 15 age-matched C3H mice fed with regular diet (RD) or AOD were exposed to filtered air (FA), a low concentration of CS (TPM 100 mg/m3; LCS) or a high concentration of CS (TPM 250 mg/m3; HCS) and survival was monitored over 16 weeks. Only the numbers of CS-exposed mice are shown because there was no death in filtered air-exposed mice. Survival curves were analyzed by Kaplan-Meier tests, using Bonferroni corrections on the Gehan-Breslow-Wilcoxon P-values. (B) Representative photomicrographs of lungs from surviving mice processed for H & E staining (10 × original magnification). (C) Quantification of emphysema scores. The values in panel C are the mean ± SEM of the emphysema score in the surviving mice in the groups (n = 8 except for 7 mice in the AOD/LCS group, 6 mice in the RD/HCS group, and 3 mice in the AOD/HCS group). The bracketed value is from a pairwise (Mann-Whitney) comparison (*P < 0.05). (D) The whole body weight of the surviving mice in each group was monitored every 2 weeks. Data are expressed as mean ± SEM.

FIGURE 2  Antioxidant diet has little effect on oxidative damage of the lungs of CS-exposed mice. (A) C3H mice fed with RD or AOD were exposed to FA, LCS or HCS for 16 weeks. The antioxidant capacity in the BALF obtained from all the 6 groups of surviving mice (n = 7 except for 4 mice in the AOD/HCS group) for 16 weeks was measured by using the trolox equivalent antioxidant content (TEAC). (B) Oxidative damage in the whole lung tissue obtained from surviving mice for 16 weeks was measured as thiobarbituric acid reactive substances (TBARS). Data are expressed as mean ± SEM.

FIGURE 2  Antioxidant diet has little effect on oxidative damage of the lungs of CS-exposed mice. (A) C3H mice fed with RD or AOD were exposed to FA, LCS or HCS for 16 weeks. The antioxidant capacity in the BALF obtained from all the 6 groups of surviving mice (n = 7 except for 4 mice in the AOD/HCS group) for 16 weeks was measured by using the trolox equivalent antioxidant content (TEAC). (B) Oxidative damage in the whole lung tissue obtained from surviving mice for 16 weeks was measured as thiobarbituric acid reactive substances (TBARS). Data are expressed as mean ± SEM.

FIGURE 3  Antioxidant diet decreases CS-induced lung inflammation. C3H mice fed with RD or AOD were exposed to FA, LCS or HCS for 16 weeks. Bronchoalveolar lavage was performed for all 6 groups of surviving mice for 16 weeks (n = 7 except for 4 mice in the AOD/HCS group). A total number of macrophages (A), neutrophils (B), and lymphocytes (C) in the BALF were measured. Data are expressed as mean ± SEM for three independent experiments.

FIGURE 3  Antioxidant diet decreases CS-induced lung inflammation. C3H mice fed with RD or AOD were exposed to FA, LCS or HCS for 16 weeks. Bronchoalveolar lavage was performed for all 6 groups of surviving mice for 16 weeks (n = 7 except for 4 mice in the AOD/HCS group). A total number of macrophages (A), neutrophils (B), and lymphocytes (C) in the BALF were measured. Data are expressed as mean ± SEM for three independent experiments.

Table 1  TEAC: % of control (mean and SEM)

Table 2  TBARS: % of control (mean and SEM)

FIGURE 4  Antioxidant diet minimally modulates metalloproteinase activity in CS-exposed mice. C3H mice fed with RD or AOD were exposed to FA, LCS or HCS for 16 weeks. The activity of pro-MMP2 (A), MMP-2 (B), and MMP-9 (C) in the BALF obtained from all the 6 groups of survived mice was measured by using zymography. Data are expressed as mean ± SEM for 3 independent experiments.

FIGURE 4  Antioxidant diet minimally modulates metalloproteinase activity in CS-exposed mice. C3H mice fed with RD or AOD were exposed to FA, LCS or HCS for 16 weeks. The activity of pro-MMP2 (A), MMP-2 (B), and MMP-9 (C) in the BALF obtained from all the 6 groups of survived mice was measured by using zymography. Data are expressed as mean ± SEM for 3 independent experiments.

Table 3  Relative band intensity

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.