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1.
Toxicol Res (Camb) ; 10(3): 542-550, 2021 May.
Article in English | MEDLINE | ID: mdl-34141168

ABSTRACT

Benzo [a] pyrene (B[a]P) is a potent mutagen and carcinogen, considered one of the commonest concomitants in the environment. The study aimed to evaluate the effect of catechin hydrate on benzo pyrene-induced kidney toxicity. Thirty-six adult male albino rats were divided into six groups: group I untreated control, group II received 10 mL/kg of corn oil (solvent of benzo [a] pyrene) twice a week, group III received 1 mL/kg 0.5% dimethyl sulfoxide (DMSO) (solvent of catechin) once per day, group IV received 50 mg/kg body weight of benzo[a]pyrene twice a week, group V received 20 mg/kg body weight of catechin in 1 mL/kg 0.5% DMSO once daily, and group VI received both catechin+benzo [a] pyrene with the same doses. All treatment was given by oral gavage for four weeks. At the end of the experiment, blood samples were collected for biochemical investigations, tissues were obtained for genotoxicity, RT-PCR, and histopathological studies. B[a]P exposure induced an increase in serum urea and creatinine levels along with severe renal histopathological changes. Our results showed a subsequent decrease in the antioxidant enzyme activities (catalase and superoxide dismutase), and conversely, (malondialdehyde) levels markedly elevated. Also, B[a]P induced DNA damage as well as activated an apoptotic pathway confirmed by upregulation of Bax, caspase-3, and downregulation of Bcl-2 expression. However, treatment with catechin-corrected kidney functions and antioxidant enzymes as well as regulated apoptosis. Histological results also supported the protective effects of catechin. These findings suggested that catechin hydrate is an effective natural product that attenuates benzo pyrene-induced kidney toxicity.

2.
Toxicol Mech Methods ; 31(6): 467-475, 2021 Jul.
Article in English | MEDLINE | ID: mdl-34027802

ABSTRACT

The major sources for human exposure to Benzo [a] pyrene (B[a]P) are contaminated food, water, and inhalation of polycyclic aromatic hydrocarbon. B[a]P is a well-known human genotoxic carcinogen (IARC Group 1). It has a tumorigenic potential in virtually all in vivo experimental animal model systems. The study aimed to evaluate the effect of catechin hydrate (CH) against B [a] P-induced toxicity in the lung of adult albino rats. Thirty-six adult male albino rats (150-200 g) were divided into six groups, three control groups, and three experimental groups: B[a] P-treated group, (CH)-treated group, and B[a] P+(CH)-treated group. At the end of the fourth week of the study, blood samples and lung tissues were obtained for the biochemical and genotoxicity, RT-PCR, histopathological, and immunohistochemical investigations, respectively. Our results clarified that B[a] P exposure caused a subsequent decrease in the activities of antioxidant enzymes (SOD, CAT), and conversely (MDA) levels elevated markedly. Also, B[a] P induced DNA damages and activated the apoptotic pathway, presented by upregulated Bax, caspase-3, and downregulated Bcl-2 gens. However, treatment with CH increased antioxidant enzymes as well as regulated apoptosis. Discernible histological changes in the lung also supported the protective effects of CH. These findings suggested that CH is an effective natural product that attenuates Benzo [a] pyrene-induced lung toxicity.


Subject(s)
Lung Diseases/chemically induced , Animals , Apoptosis , Benzo(a)pyrene/toxicity , Catechin , DNA Damage , Lung , Male , Oxidative Stress , Rats
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