PROTECTIVE EFFECT OF N-ACETYLCYSTEINE (NAC) AGAINST DI?ETHYLHEXYL PHTHALATE (DEHP) INDUCED PULMONARY TOXICITY IN MALE ALBINO RATS (HISTOLOGICAL AND IMMUNOHISTOCHEMICAL STUDY)
The Egyptian Journal of Forensic Sciences and Applied Toxicology • 2021
معلومات البحث
المؤلفون
Haidy M. Fakher1 Amina A. Farag1*, Eman M. Faruk2 , Taghrid G. Kharboush 3 , Nashwa H. Abu-Raia 4
الكلمات المفتاحية
Di-Ethylhexyl Phthalate, N-acetylcysteine, lung, lipid peroxidation; glutathione
المجلة العلمية
The Egyptian Journal of Forensic Sciences and Applied Toxicology
الناشر
Not Available
المجلد
21
العدد
1687-0875
الصفحات
89-109
publication.type
Local
رابط البحث
Open Link
المواد المرفقة
Not Available
الملخص
Di-Ethylhexyl phthalate (DEHP) is a global environmental pollutant. Human exposure to
DEHP occurs through environmental sources. Community exposure (food, air, water), as well as
medical settings’ exposure, impose crucial effects on human health. DEHP had been reported to
have cytotoxic, immunotoxic, genotoxic, and reproductive toxic properties. This work aims to
assess the possible toxic effects of DEHP on adult albino rats' lungs and to evaluate the possible
protective effects of N-acetylcysteine (NAC) using bodyweight and relative lung weight
parameters. Assessment of DHEP toxicity is measured by biochemical, histopathological, and
immunohistochemical methods. Fifty male adult albino rats were divided into five equal groups
as follows: Group Ι (Negative control group), Group ΙΙ (Positive control group), Group IΙΙ
(NAC-treated group): was given NAC orally (200 mg/kg/day), Group IV (DEHP-treated group):
was given DEHP orally (3gm/kg once daily for 4 weeks) and Group V: (DEHP + NAC-treated
group): was treated with DEHP concomitantly with NAC at the same previous doses. The results
of the present study revealed that DEHP has significantly increased the lipid peroxidation level
and significantly reduced glutathione content (GSH), superoxide dismutase (SOD) activity, and
catalase activity. The histological results of group IV showed inflammatory cellular infiltration
of the lungs associated with interstitial edema, hemorrhage, and inter-alveolar septal thickening
that were markedly reduced in group V. Also, group V, showed a significant decrease in the
collagen fibers accumulation and caspase-3 expression as compared to group IV. Conclusion:
treatment with NAC can protect against DEHP induced pulmonary toxicity in rats by decreasing
oxidative stress, inflammation, and apoptosis.
DEHP occurs through environmental sources. Community exposure (food, air, water), as well as
medical settings’ exposure, impose crucial effects on human health. DEHP had been reported to
have cytotoxic, immunotoxic, genotoxic, and reproductive toxic properties. This work aims to
assess the possible toxic effects of DEHP on adult albino rats' lungs and to evaluate the possible
protective effects of N-acetylcysteine (NAC) using bodyweight and relative lung weight
parameters. Assessment of DHEP toxicity is measured by biochemical, histopathological, and
immunohistochemical methods. Fifty male adult albino rats were divided into five equal groups
as follows: Group Ι (Negative control group), Group ΙΙ (Positive control group), Group IΙΙ
(NAC-treated group): was given NAC orally (200 mg/kg/day), Group IV (DEHP-treated group):
was given DEHP orally (3gm/kg once daily for 4 weeks) and Group V: (DEHP + NAC-treated
group): was treated with DEHP concomitantly with NAC at the same previous doses. The results
of the present study revealed that DEHP has significantly increased the lipid peroxidation level
and significantly reduced glutathione content (GSH), superoxide dismutase (SOD) activity, and
catalase activity. The histological results of group IV showed inflammatory cellular infiltration
of the lungs associated with interstitial edema, hemorrhage, and inter-alveolar septal thickening
that were markedly reduced in group V. Also, group V, showed a significant decrease in the
collagen fibers accumulation and caspase-3 expression as compared to group IV. Conclusion:
treatment with NAC can protect against DEHP induced pulmonary toxicity in rats by decreasing
oxidative stress, inflammation, and apoptosis.
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