The current study has been designed to assess the role of Persea americana (P. americana) pulp extract on potassium dichromate‐induced hepatotoxicity in rats. P. americana pulp extract administration improved the hepatic vascular congestion, blood extravasation, inflammatory cellular infiltration, Kupffer cell hyperplasia, and nuclear changes. It also significantly ameliorated hepatic interstitial and peri‐portal fibrosis and caused retrieval of the PAS‐positive reaction in the liver parenchyma and around the central vein with restoration of the glycogen granules. P. americana also significantly attenuated the immunohistochemical expression of NF‐kβ p65 and its downstream inflammatory cytokines IL6 and TNFα in the liver parenchyma. The antioxidant effect of P. americana was evidenced by significant modulation of the three major components of the thioredoxin (Trx) antioxidant system, the Trx, the thioredoxin reductase (TrxR), and the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase along with significant increase in the level of superoxide dismutase and glutathione, and decrease in the lipid peroxidation product malondialdehyde. P. americana pulp extract also caused significant elevation of hepatic protein phosphatase 5 with subsequent down‐regulation of Apoptosis signal‐regulating kinase1 (ASK1) and its downstream signaling targets MAPK kinase 4 (MKK4), p38 mitogen‐activated protein kinases (p38‐MAPKs), the c‐JUN N‐terminal kinase (JNK), and the extracellular signal‐regulated kinase 1/2 (ERK 1/2). Also, In conclusion, P. americana pulp extract has anti‐oxidative and anti‐inflammatory effects against potassium dichromate‐induced hepatotoxicity.

It can be concluded that the short period of constant light for one month had more or less no apparent effect on thyroid gland tissues while longer light periods for three months brought on detrimental outcomes on the thyroid gland structure of male albino rats.

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Background:The aim of the current work was to clarify the modulation role of green tea extract (GTE) over structural and functional affection of the thyroid gland after long term use of lithium carbonate (LC). The suggested underlying mechanisms participating in thyroid affection were researched.Materials and methods: Twenty-four Sprague-Dawley adult albino rats were included in the work. They are divided into three groups (control, LC, and concomitant LC + GTE). The work was sustained for 8 weeks. Biochemical assays were achieved (thyroid hormone profile, IL-6).Histological, histochemical (PAS) and immunohistochemical (caspase-3, TNF-α, PCNA) evaluations were done. Oxidative/antioxidative markers (MDA / GSH, SOD) and western blot evaluation of the Bcl2 family were done.Results: LC induced hypothyroidism (decrease T3, T4/increase TSH). The follicles were distended, others were involuted. Some follicles were disorganized, others showed detached follicular cells. Apoptotic follicular cells were proved (Bax and caspase-3 increased, Bcl2 decreased, Bax/Bcl2 ratio increased). The collagen fibers' content and proinflammatory markers (TNF-α and IL-6) increased. The proliferative nuclear activity was supported by increase 2 expression of PCNA. Oxidative stress was established (increase MDA/decrease GSH, SOD).With the use of GTE, the thyroid hormone levels increased, while the TSH level decreased.Apoptosis is improved as Bax decreased, Bcl2 increased, and Bax/Bcl2 ratio was normal. The collagen fibers' content and proinflammatory markers (TNF-α and IL-6) decreased. The expression of PCNA and caspase-3 were comparable to the control group. The oxidative markers were improved (decrease MDA/increase GSH, SOD). Conclusions:In conclusion, prolonged use of LC results in hypothyroidism, which is accompanied by structural thyroid damage. LC induced thyroid damage through oxidative stress that prompted sterile inflammation and apoptosis. With the use of GTE, the thyroid gland achieved its structure and function. The protecting role of GTE is through antioxidant, antifibrotic, anti-inflammatory, and antiproliferative effects.

Background: Amiodarone is a highly effective and class III antiarrhythmic drug. It can be used to treat wide range of arrhythmias. However, it is markedly concentrated in tissues leading to multiple adverse effects mainly on thyroid gland. The concomitant use of vitamin E with amiodarone in treatment of arrhythmias can ameliorate the hazardous effects of amiodarone on thyroid gland Aim of work: The aim of this work is to study the histological and ultrastructural effects of amiodarone as antiarrhythmic drug on the thyroid gland, as well as the ability of vitamin E to protect against amiodarone induced thyroid damage. Material and methods: Thirty adult male albino rats (weighing 150-200 g), were used in the study. Rats were divided into three groups (10 per group): Group A (Control group); Group B (Amiodarone treated group) and Group C (Amiodarone + Vitamin E treated group). Rats were sacrificed after 6 weeks of amiodarone administration. Thyroid gland was examined histologically and ultrastructurally. Results: Histological and ultrastructure examination of thyroid glands of rats treated with amiodarone showed disorganized follicles. Follicular epithelium showed focal disruption and desquamation. The interfollicular tissue showed increased collagen deposition. Electron microscopic examination revealed irregular nuclei, dilated rough endoplasmic reticulum and swollen mitochondria. Concomitant administration of vitamin E showed marked amelioration of hazardous effects of amiodarone with improved histologic and ultrastructural signs Conclusion: Amiodarone induces damage of the thyroid gland. Administration of vitamin E protects the thyroid gland and attenuates histopathological changes induced by amiodarone.