Akram Ranjbar

Dr. Akram Ranjbar


Research Focus & Metrics

Academic Career Length

25Years (2002-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 April 2002 in Human & Experimental Toxicology
Verified
Journal Article
Closed access
ARAkram Ranjbar
Akram Ranjbar
PPP Pasalar
P Pasalar
MAMohammad Abdollahi
Mohammad Abdollahi
Oxidative stress status and acetylcholinesterase (AChE) activity were studied in blood samples obtained from 45 organophosphorous (OP)-formulating pesticide workers with a minimum work history of 1 year in the age range of 23–55. Controls were age-matched workers of a food-making factory. They were evaluated for oxidative stress markers, including thiobarbituric acid-reactive substances (TBARS) indicator of lipid peroxidation (LPO), ferric-reducing ability of plasma (FRAP) indicator of total anti-oxidant capacity, total thiol (SH) groups and gamma glutamyl transpeptidase (GGT) levels in blood and AChE activity in erythrocytes. The results show marked inhibition of AChE activity, increased TBARS, decreased FRAP and decreased thiol group levels in workers. The reduction in activity of AChE correlated well with increased TBARS and decreased FRAP in OP formulators. It is concluded that OP-formulating workers are exposed to more oxidative stress. The measurement of erythrocyte AChE activity in pesticide workers who formulate OPs can be a good monitoring factor and is recommended to be performed in a regular manner.

1 June 2004
Verified
Journal Article
Closed access
MAMohammad Abdollahi
Mohammad Abdollahi
ARAkram Ranjbar
Akram Ranjbar
SSShahin Shadnia
Shahin Shadnia
SNShekoufeh Nikfar
Shekoufeh Nikfar
ARAli Rezaie
Ali Rezaie

1 July 2005 in Environmental Toxicology and Pharmacology
Verified
Journal Article
Closed access
ARAkram Ranjbar
Akram Ranjbar
HSHasan Solhi
Hasan Solhi
FJFarideh Jalali-Mashayekhi
Farideh Jalali-Mashayekhi
ASAlireza Susanabdi
Alireza Susanabdi
ARAli Rezaie
Ali Rezaie
MAMohammad Abdollahi
Mohammad Abdollahi

1 April 2009 in Human & Experimental Toxicology
Verified
Journal Article
Closed access
PDF file
SSS Shadnia
S Shadnia
GSG Sasanian
G Sasanian
PAP Allami
P Allami
AHA Hosseini
A Hosseini
ARAkram Ranjbar
Akram Ranjbar
MAMohammad Abdollahi
Mohammad Abdollahi
The objective of this study was to survey aluminum phosphide (AIP) poisoning in a referral poisoning hospital in Tehran servicing an estimation of 10,000,000 populations. Records of all patients admitted and hospitalized during a period of 7 years from January 2000 to January 2007 were collected and analyzed according to gender, age, cause of intoxication, amount of AIP consumed, route of exposure, time between exposure and onset of treatment, signs and symptoms of intoxication at admission, therapeutic intervention, laboratory tests, and outcome. During the studied years, 471 patients were admitted to the hospital with AIP poisoning; 50% of them were men. The overall case fatality ratio was 31%. The mean age was 27.1 years, and most of the patients were between 20 and 40 years old. Self-poisoning was observed in 93% of cases. The average ingested dose was 5.1 g, and most of the patients (73%) consumed 1–3 tablets of AIP. A wide range of symptoms and signs was seen on admission, but the most common one was cardiovascular manifestations (78.12%). The majority (65%) of patients were from Tehran. Poisoning in spring and winter (34% and 24%, respectively) was more common than other seasons. Gastric decontamination with potassium permanganate, and administration of calcium gluconate, magnesium sulfate, sodium bicarbonate, and charcoal were considered for most of the patients. Mean arterial blood pH was 7.23 and bicarbonate concentration was 12.7 mEq/L. One-hundred percent of patients with blood pH <7 died and 100% of patients with blood pH ≥ 7.35 survived. Electrocardiogram (EKG) abnormalities were noted in 65.6% of cases. There was a significant difference between survival and non-survival according to pH, HCO3 concentration, and EKG abnormality. Even without an increase in resources, there appears to be significant opportunities for reducing mortality by better medical management and further restrictions on the AIP tablets usage. Arterial blood pH seems to be a prognostic factor for the outcome of AIP-poisoned patients.

1 March 2010 in Human & Experimental Toxicology
Verified
Journal Article
Closed access
ARAkram Ranjbar
Akram Ranjbar
MGMohammad Hossein Ghahremani
Mohammad Hossein Ghahremani
MSMohammad Sharifzadeh
Mohammad Sharifzadeh
AGAbolfazl Golestani
Abolfazl Golestani
MGMahmood Ghazi-Khansari
Mahmood Ghazi-Khansari
MAMohammad Abdollahi
Mohammad Abdollahi
Objective: The objective of this study was to investigate the possible protective effects of pentoxifylline as a phosphodiesterase-5 inhibitor on malathion-induced oxidative damage to rat brain mitochondria. Methods: Rats received malathion (200 mg/kg/day) and pentoxifylline (PTX, 50 mg/kg/day) in combination or alone. Alpha-tocopherol (AT, 15 mg/kg/day) was used as a positive standard. After 1 week of treatment, blood, whole brain tissue, and brain mitochondria were isolated. The activity of enzymatic scavengers such as glutathione peroxidase (GPx), catalase (CAT), copper-zinc superoxide dismutase (Cu/ZnSOD), and manganese superoxide dismutase (MnSOD) were measured. The extents of cellular lipid peroxidation (LPO), nitrotyrosine (NOx), and the ratio of reduced versus oxidized glutathione (GSH/GSSG) were determined. The protein expression of MnSOD was determined in brain mitochondria. Results: Malathion stimulated activities of CAT, Cu/ZnSOD, GPx, and increased LPO and NOx, and decreased GSH/GSSG in whole brain homogenate. The changes in CAT, LPO, GPx, and GSH/GSSG were restored by PTX and AT. In plasma samples, malathion increased CAT, Cu/ZnSOD, and GPx activities, increased LPO, and decreased GSH/GSSG, while PTX and AT attenuated malathion-induced changes in GPx, Cu/ZnSOD, LPO, and GSH/GSSG. In brain mitochondria, malathion enhanced LPO, NOx, CAT, GPx, and MnSOD and decreased GSH/GSSG as compared to controls, whereas PTX and AT restored malathion-induced changes in GSH/GSSG, NOx, GPx, and CAT. Malathion noticeably enhanced expression of MnSOD protein as compared to controls. Malathion decreased viability of mitochondria that was recovered by AT. It is concluded that oxidative damage is at least in part the mechanism of toxicity of malathion in the mitochondria that can be recovered by PTX comparable to AT.

1 January 2006 in Evidence-Based Complementary and Alternative Medicine
Verified
Journal Article
Open access
PDF file
ARAkram Ranjbar
Akram Ranjbar
SKSara Khorami
Sara Khorami
MSMehdi Safarabadi
Mehdi Safarabadi
ASAmene Shahmoradi
Amene Shahmoradi
AMAli Akbar Malekirad
Ali Akbar Malekirad
MAMohammad Abdollahi
Mohammad Abdollahi
Medicinal plants are recognized as sources of natural antioxidants that can protect from biological system oxidative stress. The present cross‐sectional before/after clinical trial was carried out to investigate the antioxidant properties of the decoction of the flowers of Echium amoenum Fisch & C.A. Mey in humans. A group of 38 healthy subjects was invited to use the E. amoenum (7 mg kg−1) twice daily for 14 days. Blood samples before and after entering the study were measured for lipid peroxidation level (LPO), total antioxidant capacity (TAC) and total thiol (SH) molecules. A significant reduction of blood LPO (24.65 ± 11.3 versus 19.05 ± 9.7, P = 0.029) was observed after 14 days of E. amoenum consumption. Blood TAC (1.46 ± 0.51 versus 1.70 ± 0.36, P = 0.018) and total thiol molecules (0.49 ± 0.11 versus 0.56 ± 0.12, P = 0.001) increased after 14 days of E. amoenum consumption. In conclusion, this antioxidative stress potential of E. amoenum may be due to its bioactive antioxidant components, especially rosmarinic acid and flavonoids. In recent years the importance of oxidative stress in the pathophysiology of many human disorders has been confirmed, thus use of this plant as a dietary supplement is highly recommended.