<p class="abstract"><strong>Background:</strong> Adolescence is a critical period for cerebral development. Exposure to addictive substances during this phase leads to various alterations in brain functions that persist into adulthood. The present study was designed to study the neurotoxic effects of tramadol and cannabis, alone and in combination, in adolescent male albino rats by studying their behavioral, biochemical, and histopathological neurotoxic effects and their long–term consequences after withdrawal.</p><p class="abstract"><strong>Methods:</strong> <span lang="EN-IN">For this purpose, 132 adolescent male albino rats were divided into 5 groups (22 rats/ group). Group I (negative control), received only regular diet and tap water to measure the basic parameters, Group II (positive control; IIA&IIB); IIA, gavaged with normal saline. IIB, gavaged with olive oil. Group III (tramadol), gavaged with tramadol (42, 84 and 168 mg/kg/day) in the first, second and third ten days of the study respectively. Group IV (cannabis), gavaged with hashish extract (92, 184 and 368 mg/kg/day) in the first, second and third ten days of the study respectively. Group V (tramadol+cannabis), gavaged with tramadol and hashish extract in the same doses as Group III&IV. By the end of the first month, the half number of rats was subjected to performing behavior tests. Specimens from the brain were taken for performing biochemical and histopathological studies. All remaining rats were held for another 4 weeks non–dosing spontaneous recovery period after withdrawal of the treatment and were evaluated again by the same previous parameters.</span></p><p class="abstract"><strong>Results:</strong> Abuse of tramadol or cannabis, alone and in combination, caused antidepressant effect (sucrose preference test), impaired spatial memory (Morris water maze), elevated serotonin levels in the cerebral cortex and hippocampus, induced oxidative stress (significantly elevated malondialdehyde level and reduced catalase activity) as well as deleteriously altered brain histopathology and marked increase in brain Caspase–3 expression. However, abuse of both tramadol and cannabis conferred more antidepressant effect but more neurotoxic effect. After withdrawal, the antidepressant effect was reversed, no improvement of the spatial memory, marked depletion of 5–HT, more improvement in antioxidants and apoptotic markers and incomplete regression of brain histopathological alteration resulted.</p><p class="abstract"><strong>Conclusions:</strong> <span lang="EN-IN">Abuse of tramadol and cannabis, alone and in combination, induced neurotoxicity which proved behaviorally, biochemically and histopathologically.</span></p>
Lead poisoning has been known as an important disorder that affects individuals through acute, sub-acute and chronic exposure in environmental and occupational settings. This study was conducted to compare the curative role of garlic combined with silymarin versus dimercaptosuccinic acid (DMSA) in decreasing lead induced nephrotoxicity in adult male albino rats. The period of lead intoxication extended for 3 months followed by either 1 month treatment with garlic and silymarin or 5 days treatment with DMSA. Lead poisoning caused non-significant difference in kidney function tests (BUN and serum creatinine) while, it caused significant elevation in kidney lead level, significant decrease in renal antioxidant enzyme glutathione peroxidase and significant elevation in kidney malondialdehyde. Histologically, lead induced disorganization and shrinkage of glomeruli with sloughing and vaculation of epithelium, widening of Bowman's space and inflammatory infiltration in renal medulla. Treatment by garlic extract combined with silymarin as well as treatment with DMSA resulted in significant improvement in the affected parameters. Also, both methods of treatment resulted in improvement of the histopathological changes. It can be concluded that garlic extract combined to silymarin is comparable to DMSA in amelioration of lead induced nephrotoxicity.
Ginger is a world known food plant which is equally reputed for its medicinal properties. The aim of the work is to study the acute and subacute cardiovascular toxicity of ginger in adult male albino rats and its possible mechanisms of action. The in-vivo studies included eighty four adult male albino rats for the acute and subacute toxicity experiments. The rats were divided into 7 groups each one consisted of 12 rats. All rats received ginger orally in saline. Each of the in-vivo studies included 2 control groups, the negative and positive control rats. In the acute toxicity study, rats received ginger in a single dose of 2500 mg/ kg. In the subacute toxicity study group VI and VII received ginger in a daily dose of 50 mg/ kg and 500 mg/ kg respectively for 28 days. After 24 hours of the acute toxicity and 28 days of the subacute experiments six rats of each group were used for blood pressure and heart rate recording. The other 6 rats were used for histopathological study of the cardiac tissue. The in-vitro experiments included 6 rabbits each weighing 1.5-2 kg. Ginger (5mg/ml) was incubated with the aortic spiral strip of each rabbit to investigate the possible mechanisms of action of Ginger. It was concluded that; single dose of 2500 mg/ kg ginger can be a toxic by causing severe hypotension and bradycardia with induction of prenecrotic changes in cardiac tissue. The administration of ginger in a dose of 50 mg/ kg for 28 days produced bradycaria with waviness in cardiac muscle fibers. Ginger in a dose of 500 mg/ kg produced both hypotension and bradycardia with degenerative changes in cardiac myocyte tissue. The hypotensive and bradycardic effects of ginger may be partially due to induction of vasodilatation by increasing nitric oxide release or synthesis and partially due to a calcium channel blocking effect. Also, a cholino-mimetic effect could be contributed in the cardiovascular effects of ginger. While the In-vitro results revealed that ginger is a partial vasorelaxant as it produced a relaxant effect on rabbit's aortic strip procontracted with phenylephrine, while preincubation with L-nitroarginine methyl ester (L-NAME) significantly attenuated the ginger-induced relaxation indicating that the vasodilator effect of ginger is partially mediated through nitric oxide synthesis or release from L-NAME.
Fungicides are pesticides that specifically, in agriculture, used to protect fruits and vegetables during storage or are applied directly to ornamental plants, trees, field crops, cereals and turf grasses. Mancozeb (MZ), a broad spectrum dithiocarbamate fungicide used in Egypt, is one of the most frequently utilized pesticides in homes, agricultural, and industrial settings worldwide. The main mechanism of mancozeb toxicity is the creation of reactive oxygen species and the activation of oxidative stress, which leads to mitochondria dysfunction, apoptotic pathways activation and increase lipid peroxidation that are implicated in the pathophysiology of numerous diseases and has been linked to acute and chronic exposure to such dithiocarbamates pesticides. The purpose of this review article is to highlight on MZ regarding chemical structure, environmental fate, ways of human exposure, mechanism of toxicity and some of its potential health hazards. So, it is important to recommend the presence of an applicable access of information for farmers and workers about proper use or the precautions needed when handling pesticides or at least using the simplest hygienic and protective measures, also, attention to sanitary environmental work place is required to avoid take-home mechanism of toxicity. Also, widespread public education regarding the health hazards of dithiocarbamates pesticides is essential.
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