Iranian Journal of Toxicology
Volume:15 Issue: 4, Oct 2021

Body packing and body stuffing of illicit drugs have increased in recent decades. The drug contents of the packages vary from region to region, and there are controversies surrounding the diagnostic and therapeutic methods. The aim of this study was to explore the clinical presentations, diagnostic and therapeutic measures, and the subsequent clinical outcomes of drug concealment by people.

A retrospective analysis was performed on data for all cases of body packing and body stuffing that were referred to a university hospital, in Isfahan, Iran, from Mar. 2013 to Feb. 2018. 

Sixty-eight body stuffers and 18 body packers (n=86) were included in this study. Seventy-eight patients (90.7%) were male, mostly aged between 20 to 40 years. There was no significant difference between the two groups with respect to the signs and symptom, hospital stay, treatment and clinical outcomes. Heroin and crystal methamphetamine, n=52 (60%) and n=22 (25%), respectively, were the most substances detected, irrespective of the concealment method. Abdominal X-ray and CT scan tests were positive for the detection of at least one packet in each of the 94.4% of the patients.

Heroin and crystal methamphetamine were the most common substances concealed in the bodies of the patients. Based on our findings, CT scan was more sensitive than abdominal X-ray test in the detection of illicit drug packets concealed in the patients. Close observation and whole bowel irrigation were effective therapeutic modalities in most cases. All cases were fully recovered and discharged from the hospital.

The protective effects of Montelukast (Mont), as an anti-inflammatory drug, against cadmium-induced kidney cell damage have already been studied and identified. Since the significant part of cadmium nephrotoxicity is caused by oxidative stress, this in vivo and in vitro study was conducted to investigate the possible role of Montelukast antioxidant properties in the protection. 

In the in vivo section, 42 rats were treated in seven groups of six rats as follows: Control; Cadmium Chloride (CdCl2) control; Montelukast control; CdCl2 plus Montelukast treatment; CdCl2 with Montelukast pre-treatment; Vitamin E control; CdCl2 plus Vitamin E treatment. In the in vitro section, human embryonic kidney cells (HEK293) were treated with CdCl2; Montelukast; Combined CdCl2 and Montelukast; Vitamin E; Combined CdCl2 and Vitamin E. 

Montelukast, in both treatment and pretreatment forms, reduced serum urea, creatinine, and potassium levels compared to CdCl2 group, in vivo. Similar to vitamin E, the pre-treatment with Montelukast was associated with a significant decrease in Nitric Oxide (NO) and Total Antioxidant Capacity (TAC) in serum and renal tissue, and a significant increase in Glutathione Peroxidase (GPX) activity in serum compared those in the CdCl2 group. In the in vitro section of the study, Montelukast significantly reduced Malondialdehyde (MDA) and NO while the TAC level, Superoxide Dismutase (SOD), and the GPX activity increased significantly.

Overall, the antioxidant effects of Montelukast appear to play a prominent role in preventing the renal toxicity due to cadmium exposure.

Oxymetholone, an anabolic-androgenic steroid, has been used to treat some diseases. The abuse of this compound, especially for muscle growth, has severe oxidative side effects on the liver and kidneys. Oxidative stress and free radicals are responsible for the development of various diseases. Phytochemicals are sources of polyphenols, flavonoids, saponins, etc. and may act as scavengers of free radicals. Saffron (Crocus sativus) has considerable antioxidant properties, which may be useful in reversing or preventing these negative effects.

To evaluate the effects of saffron on the liver and kidneys degenerative changes induced by oxymetholone, 24 male Wistar rats were used. The rats were randomly divided into four groups of six rats each as: a) sham (normal saline, 40 mg/kg/day), b) saffron control (40 mg/kg/day), c) oxymetholone (50 mg/rat), and d) treatment group [saffron (40 mg/kg/day)+oxymetholone (50 mg/rat)]. The course of examination was 30 days.

After one month, the sham and saffron control groups had normal histological findings. The treatment group with saffron showed a significant reduction in the hepatic and renal degenerative changes induced by oxymetholone compared to those observed in group.

Based on the histopathological results, the use of saffron produced protective effects against the degenerative changes in rats’ liver and kidneys induced by oxymetholone.

Damages to the peripheral fibers of sensory nerve cells and central neurons cause neuropathic pain. Manifestations of neuropathic pain occur in various conditions, including diabetes mellitus, chemotherapy, and as the side effects of some medications. Cressa cretica has long been used in traditional medicine for pain control. This study was conducted to determine the role of opioid receptors in the analgesic effect of the hydroalcoholic extract of C. cretica in an experimental model of neuropathic pain.

The hydroalcoholic extract of C. cretica was prepared, and its total phenolic and flavonoid contents were standardized. Painful peripheral neuropathy was induced in rats by Chronic Constriction Injury (CCI) of the sciatic nerve. To evaluate the effects of the extract, the animals were orally given C. cretica extract (300 mg/kg), gabapentin (70 mg/kg) or normal saline (4 mL/kg) on days 3, 7, 14, and 21 after surgery, and behavioral tests were performed 45 minutes after taking the medications. To evaluate the role of the opioid receptors, Naloxone (1 mg/kg, IP) was given to rats treated with the extract 30 minutes after the extract and then the behavioral tests were performed after 15 minutes.

The hydroalcoholic extract of C. cretica attenuates neuropathic pain induced by CCI in rats. The extract works acutely and chronically, depending on the dosage and duration of use.

The hydroalcoholic extract of C. cretica reduces CCI-induced neuropathic pain in rats, and Naloxone, as an opioid receptor antagonist, inhibits this effect.

Although ethanol exerts its neurotoxic effect on the brain through inflammatory and oxidative processes, the effect of Riboceine on the brain following ethanol neurotoxicity is yet to be elucidated. Therefore, this study was designed to evaluate the effects of riboceine on the cellular, behavioral, and molecular impairments induced by ethanol toxicity in rats.

A total of 24 male Wistar rats weighing between 160-170 grams were used for the study, and were divided into four groups of six rats each. After completion of the administration of ethanol and riboceine, and testing for motor impairment, the rats were sacrificed. The cerebellum was excised and processed for oxidative stress analyses, based on oxidative stress markers and histological examinations. The immunohistochemical expression of astrocytes in the cerebellum was examined, using Glial Fibrillary Acidic Protein (GFAP) stain. 

This study demonstrated that ethanol-induced neurotoxicity in the cerebellum, characterized by increased oxidative stress profile, astrocyte activation, and neuronal death in the cerebellum, especially the Purkinje layer. Necrosis, significant decrease in Superoxide Dismutase (SOD), Catalase (CAT) and Gluathione (GSH) activities (P<0.05) as well as astrogliosis was associated with ethanol treatment. However, riboceine was observed to significantly increase the cerebellar SOD, CAT and GSH activities with significantly reduced Malondialdehyde (MDA) levels (P<0.05). It also attenuated the histomorphological alteration of the cerebellum and reduced the cerebellar astrocytes activation following ethanol-induced neurotoxicity, thus leading to the attenuation of motor impairment. 

Riboceine attenuated motor impairment caused by chronic ethanol-induced neurotoxicity, suggestive of its anti-oxidative and anti-inflammatory properties.

Nitrate content is one of the most critical factors to determine the quality of vegetables, and its permissible limits in food chain is important to the human health. Due to the harmful effects of nitrate, many studies have been conducted on its accumulation in crops in recent years. This study assessed the nitrate concentrations in some edible vegetables and the associated health risks. 

In this descriptive study, raw agricultural produce, such as leafy vegetables, tubers, cucurbits, kitchen produce and edible grains were collected in the winter and summer. The samples were then transferred to a laboratory by maintaining the temperature-controlled supply chain. After preparing the samples, the nitrate content was determined in each, using an Ultraviolet-Visible spectrophotometric (UV/Vis) unit. The data were analyzed statistically on SPSS v. 26.

The mean nitrate contents in leafy and kitchen produce, grains, and tuber vegetables were approximately 130, 48, 101, and 61ppm, respectively. The average nitrate content in the winter was around 38ppm and in the summer about 44 ppm. The highest nitrate content was documented in spinach (1100.15 ppm) and the lowest in tomatos (20.97 ppm).

The results indicated that the highest nitrate content was found in leafy produce grown in northern Iran. The highest health risk for non-carcinogenic conditions was likely to be linked to the consumption of spinach and other edible vegetables, wheat, rice, and potatoes.

Acetaminophen is a popular antipyretic and analgesic medication worldwide; however, its therapeutic window is narrow, which may lead to overdose or toxicity. This study was conducted to assess the correlation between the serum acetaminophen levels before and 4 hours after the acute toxicity with this drug. The objective of this study was to test the validity of the serum level to arrive at a clinical decision on the toxicity with acetaminophen.

This cross-sectional study was performed on patients hospitalized and treated with a diagnosis of acute acetaminophen overdose during one year (Sept. 2018 to Sept. 2019) at the Toxicology Department of Imam Reza Hospital, Mashhad, Iran. Patients were analyzed for demographics, time of ingestion, their first and second serum acetaminophen concentrations. 

A total of 204 patients (106 male & 98 female) were included in this study. The average dose of acetaminophen ingestion by these patients was 14.5±3.50 g and all patients were treated successfully with N-Acetyl-Cysteine (NAC). The variables of age (P=0.293), serum acetaminophen levels at 1-2 h (P=0.679), and at 2-3 h (P=0.126) did not have significant relationships with the serum acetaminophen level on the fourth hour. However, the serum acetaminophen levels tested between 3-4 h and acetaminophen intoxication dosage had significant relationships with the acetaminophen level on the fourth hour.

In patients with acute acetaminophen toxicity, the data on the serum levels obtained before a 4-hour timepoint from the ingestion were not useful to decide on the need for the rescue treatment with N-acetyl-cysteine.

Epilepsy is a neurological disorder caused by uncontrollable discharge of action potentials from neurons in the brain. After a seizure, oxidative stress may cause a significant neuronal damage. In the current study, we assessed the anticonvulsant and antioxidant properties of pioglitazone, a peroxisome proliferated activated receptor-γ (PPAR-γ) agonist that is used in type-2 diabetes, on pilocarpine-induced seizure in mice. 

Pilocarpine (400 mg/kg) or normal saline was injected intraperitoneally 4 hours after oral administration of Pioglitazone (80 mg/kg). Also, carboxymethyl cellulose was administered orally in control and Pilocarpine groups. After the administration of Pilocarpine all of the mice were observed for 1 hour to measure the seizure latency time. Pilocarpine-induced seizures were categorized using the Racine scale. Then all animals were decapitated, brain was removed and hippocampus was dissected. Finally, the level of Malondialdehyde (MDA) and Catalase (CAT) activity, Superoxide Dismutase (SOD), and Glutathione Reductase (GR) levels were quantified in hippocampus by biochemical methods.

Pioglitazone significantly increased the latency to seizure onset of stages 1-4 (P≤0.01-0.001). Also, pioglitazone prevented the development of stage 5 of the pilocarpine-induced seizure. After the seizure, pioglitazone significantly decreased the level of MDA (P<0.01) and elevated the levels of CAT (P<0.01), SOD (P<0.01) and GR (P<0.001) enzymes in the mice hippocampus compared to those in the pilocarpine group.

The findings of this study indicate that the antioxidant effect of pioglitazone may play an important role in its protective effects against neuronal damage caused by pilocarpine-induced seizure.