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1.
Histochem Cell Biol ; 161(6): 477-491, 2024 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-38641701

RESUMO

Chemotherapy-induced alopecia (CIA) represents one of the most severe side effects of chemotherapy, which forces some patients to reject cancer treatment. The exact pathophysiological mechanisms of CIA are not clearly understood, which makes it difficult to discover efficient preventive or therapeutic procedures for this adverse effect. N-acetylcysteine (NAC) has a strong antioxidant activity as it stimulates glutathione synthesis and acts as an oxygen radical scavenger. The current study tried to investigate the efficacy of NAC in preserving biochemical parameters and hair follicle structure against cyclophosphamide (CYP) administration. In total, 40 adult female C57BL/6 mice were induced to enter anagen by depilation (day 0) and divided into four groups: group I (control), group II (CYP) received a single dose of CYP [150 mg/kg body weight (B.W.)/intraperitoneal injection (IP)] at day 9, group III (CYP & NAC) received a single dose of CYP at day 9 as well as NAC (500 mg/kg B.W./day/IP) from day 6-16, and group IV (NAC) received NAC from day 6-16. CYP administration in group II induced an increase in malondialdehyde (MDA), decrease in superoxide dismutase (SOD), histological hair follicle dystrophy, disruption of follicular melanogenesis, overexpression of p53, and loss of ki67 immunoreactivity. NAC coadministration in group III reversed CYP-induced alterations in the biochemical parameters and preserved hair follicle structure, typical follicular melanin distribution as well as normal pattern of p53 and ki67 expression. These findings indicated that NAC could be used as an efficient and safe therapeutic option for hair loss induced by chemotherapy.


Assuntos
Acetilcisteína , Alopecia , Ciclofosfamida , Modelos Animais de Doenças , Folículo Piloso , Camundongos Endogâmicos C57BL , Animais , Alopecia/induzido quimicamente , Alopecia/tratamento farmacológico , Alopecia/patologia , Alopecia/metabolismo , Camundongos , Folículo Piloso/metabolismo , Folículo Piloso/efeitos dos fármacos , Folículo Piloso/patologia , Feminino , Acetilcisteína/farmacologia , Antineoplásicos Alquilantes
2.
J Mol Histol ; 53(3): 523-542, 2022 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-35118589

RESUMO

Etoposide (Eto) is an anti-cancer drug that is associated with serious adverse effects on male reproductive function. Omega-3 polyunsaturated fatty acids (ω-3 PUFAs) and selenium (Se) are known as anti-inflammatory, anti-apoptotic and anti-oxidant agents. This work was designed to investigate changes in the biochemical parameters as well as alterations in Sertoli cell vimentin expression, ultrastructure and ectoplasmic specializations (ESs) following Eto treatment and to assess the ameliorative effect of ω-3 versus Se on these alterations. Eighty four adult male albino rats were used and classified into four groups: group I (control group), group II (Eto group) received Eto in a single intra-peritoneal (IP) dose (60 mg/kg B.W.), group III (Eto & ω-3 group) received the single IP dose of Eto as well as ω-3 (300 mg/kg B.W./day by intra-gastric intubation) starting 5 days before Eto injection till the time of sacrifice & group IV (Eto & Se group) received the single IP dose of Eto as well as Se (0.5 mg/kg B.W./day IP) starting 5 days before Eto injection till the time of sacrifice. The rats were subdivided into 2 subgroups (a) and (b) that were sacrificed 3 and 7 days after Eto injection respectively. Eto administration in group II induced increase in malondialdehyde (MDA), decrease in superoxide dismutase (SOD), collapse of Sertoli cell vimentin filaments and ultrastructural degenerative changes in both Sertoli cells and ESs. Se (group IV) reversed Eto toxic effects potently, while ω-3 (group III) had some limited protective effects.


Assuntos
Selênio , Células de Sertoli , Animais , Masculino , Elétrons , Etoposídeo/metabolismo , Etoposídeo/farmacologia , Selênio/metabolismo , Selênio/farmacologia , Células de Sertoli/metabolismo , Testículo/metabolismo , Vimentina/metabolismo , Vimentina/farmacologia , Ratos
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