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1.
Niger J Physiol Sci ; 38(2): 201-209, 2023 Dec 31.
Article in English | MEDLINE | ID: mdl-38696680

ABSTRACT

Long-term antiretroviral drug toxicity may exacerbate the impact of HAART-Cyperus esculentus (C. esculentus) interactions on testicular function in HIV-infected individuals. This study examined the ability of C. esculentus plants to treat testicular dysfunction, which is thought to be a probable side effect of antiretroviral toxicity. Adult Wistar male rats weighing 90-110 g were divided into six groups and administered the prescribed treatments. In addition to testicular histology and stereological parameters, testosterone levels, follicle-stimulating hormone levels, antioxidant markers, malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione levels were also evaluated. The adverse consequences of highly active antiretroviral therapy (HAART) include considerable loss of germ cells, enlargement of the tubular lumen, widening of interstitial gaps, and severe hypocellularity. Compared to the other treatment groups, MDA levels dramatically increased, whereas GSH and antioxidant enzyme (SOD) levels significantly decreased. Testicular architecture was largely conserved after treatment with C. esculentus, with a notable increase in the cellular densities of germinal and interstitial cells and a notable decrease in the tubular lumen. Vacuolation, architectural malformations, and hypoplastic changes were reduced. Significant improvements were also observed in C. esculentus in terms of elevated antioxidant SOD and GSH levels and decreased MDA levels. C. esculentus reduced architectural distortions and testicular dysfunction caused by HAART, and improved testicular morphology. Further exploration of these pathways is required.


Subject(s)
Cyperus , Rats, Wistar , Testis , Animals , Male , Testis/drug effects , Testis/pathology , Testis/metabolism , Rats , Plant Extracts/pharmacology , Testosterone/blood , Superoxide Dismutase/metabolism , Antioxidants/pharmacology , Antioxidants/metabolism , Glutathione/metabolism , Antiretroviral Therapy, Highly Active , Malondialdehyde/metabolism , Oxidative Stress/drug effects , Anti-Retroviral Agents/toxicity
2.
Hum Exp Toxicol ; 41: 9603271221149010, 2022.
Article in English | MEDLINE | ID: mdl-36572547

ABSTRACT

Ethanol exposures have been reported to disrupt the development of the retina and optic nerve which can be considered as part of underlying mechanisms of visual pathway impairments. This study aims to investigate the cellular integrity of the retina and the expression of melatonin receptor (MTNR1A) in the retina when assaulted chronically and simultaneously by ethanol and acetaminophen. Animals were randomly grouped into five groups. Control (normal saline), Alcohol group (25% alcohol in 2% sucrose solution), Acetaminophen group, (100 mg/kg BW for 14 days), Acetaminophen + Alcohol group (25% alcohol in 2% sucrose solution + 100 mg/kg BW of paracetamol). Withdrawal group (25% alcohol in 2% sucrose solution + 100 mg/kg BW of paracetamol). The body weight and rectal temperature of the animals were taking every 2 days and a post mortem study was conducted by quantitatively assessing the markers of oxidative stress. Melatonin level was quantified in the retina tissue and Immunohistochemistry was done via MTNR1A to study the expression of melatonin receptor type 1A in the retina. These results demonstrate that alcohol and acetaminophen significantly reduced the activity of retina rat melatonin (MTNR1A) levels, lowers the SOD and MDA activity. Expression of MTNR1A was reduced in the ganglionic cell layer of Alcohol and acetaminophen group as compared to the control and withdrawal group. It can be inferred that chronic simultaneous intake/consumption of alcohol and acetaminophen altered the melatonin level in the retina and this may implicate the circadian clock and melatonin in Wistar rat visual system.


Subject(s)
Melatonin , Animals , Rats , Melatonin/pharmacology , Acetaminophen/toxicity , Ethanol/toxicity , Receptor, Melatonin, MT1/metabolism , Rats, Wistar , Retina/metabolism
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