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Hepatocellular carcinoma (HCC) accounts for more than 5% of all human cancers. Diacerein (DIA), an interleukin (IL)-1β inhibitor, is used for the treatment of osteoarthritis. DIA is a potential anticancer drug acting on several protein targets in the process of apoptosis. The present study aimed to explore the molecular mechanisms underlying the effect of DIA in the treatment of trichloroacetic acid (TCA)–induced pre-neoplastic changes in rats. Rats were allocated into 5 groups and treated for 4 weeks. Group 1: control; received vehicle, Group 2: TCA group; received TCA (1 g/kg, orally for 5 days). Group 3: DIA-treated group; received TCA +DIA (50 mg/kg/day, orally, for 4 weeks). Group 4: positive control group; received TCA (1 g/kg, orally, for 5 days) + 5-fluorouracil (5-FU) (75 mg/kg) intraperitoneally (i.p.), for 4 weeks as a standard anticancer drug. Group 5: received TCA (1 g/kg, orally for 5 days) + DIA (50 mg/kg/day, orally, for 4 weeks) + 5-FU (75 mg/kg, i.p., for 4 weeks). Serum liver enzymes, oxidative stress parameters, inflammatory parameter (IL-1β), and angiogenesis marker vascular endothelial growth factor (VEGF) were assessed along with histopathological evaluation. An apoptotic marker as caspase-3 expression was measured by western blot analysis. Immunoexpression of proliferating cell nuclear antigen (PCNA) and hypoxia-inducible factor-1α (HIF-1α) was evaluated. Results and conclusion: The outcomes proved that at histological level, DIA ameliorated hepatic precancerous lesion via modulation of IL-1β–HIF-1α–VEGF pathway. Conclusion IL-1β mediates angiogenesis indirectly, as it has been shown to induce hypoxia-inducible factor-1α (HIF-1α) which upregulates VEGF.

Background Methotrexate (MTX), an anticancer drug, has been linked to multiple organ toxicity. The drug-induced acute toxic symptoms can negatively affect the patient's commitment to the course of treatment. Materials and methods This study aimed to investigate the mitigating action of agomelatine (Ago) against MTX-induced lung and intestinal toxicity. Forty eight male Wister rats were randomized into six experimental groups: Group 1: Control; Groups 2 and 3: received Ago LH Group 4: received MTX 10 mg/kg/day, i.p. on days 7-9; Group 5: received Ago L (20 mg/kg) + MTX; Group 6: received Ago H (40 mg/kg) +MTX. The duration of the study was 10 days. Lung/intestine oxidative markers were measured. Lung/intestinal tissues IL-6, STAT3, and HO-1 levels were evaluated by ELISA. Besides, lung/intestinal tissues were examined for Histological changes, collagen fibers detection using Massonꞌs trichome stain, and immunohistochemical study using HSP70 antibody. Results MDA, NOx, IL-6, and STAT3 levels were significantly higher in the MTX group's lungs and intestines, indicating lung and intestinal toxicity. There were substantial decreases in GSH, SOD tissue levels, and HSP 70 immunoexpression, as well as histological changes suggesting significant lung and intestinal injury. All of the above parameters improved significantly by using Ago. Conclusion By reducing oxidative stress, inflammatory processes, and modulating the IL-6/STAT3 pathway, Ago has potent ameliorative effects against MTX-induced lung/intestinal toxicities.

Hydrogen sulfide (H(2)S), along with nitric oxide (NO) and carbon monoxide (CO), proved to have renoprotective effects in various renal diseases. Therefore, this study investigated the renoprotective effect of H(2)S, in a renal injury model, and its crosstalk with other gasotransmitters such as CO. Thirty-two adult rats were divided into four groups: control, gentamicin (GEN)-treated, GEN + sodium hydrosulfide (NaHS), and GEN + NaHS + zinc protoporphyrin (ZnPP) groups. GEN was used to induce renal injury, NaHS is a water-soluble H(2)S, and ZnPP is a selective heme oxygenase-1 (HO-1) inhibitor used to inhibit CO synthesis in vivo. NaHS improved kidney functions in the GEN group as evidenced by significantly lower levels of renal injury markers: serum urea, creatinine, uric acid, urinary albumin excretion, and urinary albumin/creatinine. Moreover, NaHS administration to the GEN-treated group significantly lowered renal levels of NO and tumor necrosis factor-α with an increase in total antioxidant, HO-1, and interleukin-10 levels. Furthermore, NaHS administration downregulated the GEN-induced overexpression of the renal inducible nitric oxide synthase (iNOS) and upregulated the suppression of endothelial nitric oxide synthase (eNOS) with improvement in the histological examination and periodic acid Schiff (PAS) staining. However, this improvement in kidney function produced by NaHS was reduced by combination with ZnPP but still improved as compared with the GEN-treated group. The renoprotective effects of H(2)S can be through its effects on renal tissue antioxidants, pro-inflammatory and anti-inflammatory cytokines, and expression of eNOS and iNOS which can be partially dependent on CO pathway via induction of HO-1 enzyme.

Objectives Acute pancreatitis (AP) is a common severe critical illness with a high mortality rate. We aimed to study the effect of vinpocetine (Vinpo) in the treatment of AP because of its anti-inflammatory, antioxidant, and antiapoptotic effects. Materials and methods Thirty two adult male albino Wistar rats were randomized to four groups: control group, Vinpo group (20 mg/kg.P.O.), l -arginine group (two intraperitoneal injections of l -arginine 2.5 g/kg, 1 h apart), and Vinpo + L-arginine group. Vinpo administration was once daily for 7 consecutive days and started 1 h later after l -arginine administration. We measured serum enzyme biomarkers (lipase and amylase), levels of pancreatic malondialdehyde (MDA), total antioxidant capacity (TAC), reduced glutathione (GSH), total sulfhydryl (T-SH), total nitrite/nitrate (NOx), Interluken-6 (IL-6), tumor necrosis factor-alpha (TNF-α), Nuclear factor (erythroid-derived 2)-like 2 (Nrf2), Sirtuin type 1 (Sirt1), and caspase-3 activity. Furthermore; histological changes, anti-insulin, and inducible nitric oxide synthase (iNOS) immuno-expressions were examined. Results l -arginine group displayed AP as manifested by a significant increase in serum lipase and amylase, MDA, NOx, IL-6, TNF-α, caspase-3 with iNOS immuno-expression. Histological changes indicating marked pancreatic injury were observed together with a significant decrease in TAC, GSH, T-SH, Nrf2, Sirt1 levels, and anti-insulin immuno-expression. Vinpo showed a significant amelioration in all parameters. Conclusion Vinpo possesses potent ameliorative effects against AP by decreasing oxidative stress, inflammatory process, and apoptosis through regulation of the Sirt1/Nrf2/TNF-α pathway.

Purpose: Cancer rates have been increased among women of reproductive age nowadays. Hence, many young female will be exposed to chemotherapeutic agents as cyclophosphamide (CP), carrying the hazard...

Introduction The study aimed at investigating the hepatic effect of direct acting anti-hepatitis C virus drugs (DAAs), sofosbuvir (Sof) and daclatasvir (Dac), in thioacetamide (TAA)-induced liver injury in rats. Material and methods Animals were allocated to 7 groups: a normal control group, a TAA group (receiving TAA 50 mg/kg, i.p. twice weekly), two TAA groups receiving either a low or a high dose of Sof (Sof-L and Sof-H; 41.1 mg/kg and 82.2 mg/kg, respectively), two TAA groups receiving either a low or a high dose of Dac (Dac-L and Dac-H; 6.2 mg/kg and 12.4 mg/kg, respectively), and a TAA group receiving both Sof-L and Dac-L. Results After 6 weeks, TAA significantly elevated the serum activities of liver enzymes, along with histopathological evidence of liver injury. These findings were associated with a significant increase in a fibrotic marker (tissue inhibitor metalloproteinase-1 - TIMP-1), proinflammatory cytokine (tumor necrosis factor alpha - TNF-α), and oxidative stress parameters (malondialdehyde [MDA] content, and superoxide dismutase [SOD] and catalase activities) in hepatic tissue. TAA rats treated with Sof-L, Dac-L, Dac-H and a combination of Sof-L plus Dac-L showed significant amelioration of TAA-induced liver injury. Their effects were accompanied by a significant reduction in TIMP-1, TNF-α and oxidative stress parameters in hepatic tissue. Interestingly, Sof-H caused no improvement in TAA-induced hepatic injury. Conclusions The hepatic effects of Sof and Dac in TAA-induced liver injury appeared to be mediated by anti-oxidant effects, and inhibition of TNF-α and TIMP-1.

Objective. The aim of the current study was to assess the protective outcome of hemin, a heme oxygenase-1 (HO-1) inducer on L-arginine-induced acute pancreatitis in rats. Acute pancreatitis (AP) is considered to be a critical inflammatory disorder with a major impact on the patient health. Various theories have been recommended regarding the pathophysiology of AP and associated pulmonary complications.Methods. Twenty-four adult male albino rats were randomly divided into four groups: control group, acute pancreatitis (AP), hemin pre-treated AP group, and hemin post-treated AP group.Results. Administration of hemin before induction of AP significantly attenuated the L-arginine- induced pancreatitis and associated pulmonary complications characterized by the increasing serum levels of amylase, lipase, tumor necrosis factor-α, nitric oxide, and histo-architectural changes in pancreas and lungs as compared to control group. Additionally, pre-treatment with hemin significantly compensated the deficits in total antioxidant capacities and lowered the elevated malondialdehyde levels observed with AP. On the other hand, post-hemin administration did not show any protection against L-arginine-induced AP.Conclusions. The current study indicates that the induction of HO-1 by hemin pre-treatment significantly ameliorated the L-arginine-induced pancreatitis and associated pulmonary complications may be due to its anti-inflammatory and antioxidant properties.

To investigate the effect of Ginsenoside-Rb1 (GRb1) on lithium (Li+)-induced toxicity, GRb1 was given to rats orally (100mg/kg) for 14days. In independent groups, lithium chloride (4meq/kg/day i.p.) was administered at day 4 of the experiment for 10days, with or without GRb1. Li+ caused significant deterioration of behavioral responses including righting reflex, spontaneous motor activity and catalepsy. Li+ also caused distortion in normal renal, cerebral and cerebellum architecture and significantly worsened all kidney functional parameters tested compared to control. In addition, Li caused oxidative stress in both kidney and brain, evident by significant increase in malondialdehyde and nitric oxide levels, with decrease in reduced glutathione and catalase activity. Administration of GRb1 prior to Li+ significantly improved behavioral responses, renal and brain histopathological picture, kidney function tests and oxidative stress markers compared to sole Li+-treated group. Concomitant administration of GRb1 decreased Li+ levels by about 50% in serum, urine and brain and by 35% in the kidney. Interestingly, Li+ had a differential effect on cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) pathway, as it significantly increased COX-2 expression and PGE2 level in the kidney, while decreasing them in the brain compared to control. On the other hand, administering GRb1 with Li+ suppressed COX-2/PGE2 pathway in both kidney and brain compared to Li+ alone. In conclusion, GRb1 can alter Li+ pharmacokinetics resulting in extensively decreasing its serum and tissue concentrations. Furthermore, COX-2/PGE2 pathway has a mechanistic role in the nephro- and neuro-protective effects of GRb1 against Li+-induced toxicity.

One of the major obstacles that males with diabetes may confront is subfertility or infertility. Thus, the present study investigated the effect of co-administration of metformin and zinc (Zn) on the testes of streptozotocin-induced diabetic rats. Male albino rats were randomly divided into 4 groups: control group; untreated diabetic group; diabetic + metformin group, in which diabetic rats were treated orally with metformin (250 mg/kg) once daily for 4 weeks; and diabetic + metformin + Zn group, in which diabetic rats were treated orally with metformin in combination with Zn (10 mg/kg) once daily for 4 weeks. Concomitant administration of metformin and Zn produced a significant decrease in serum levels of glucose and insulin and testicular levels of malondialdehyde and tumor necrosis factor α. Additionally, there was a significant increase in serum levels of Zn, testosterone, and follicle-stimulating hormone, as well as testicular total antioxidant capacity and anti-apoptotic protein Bcl-2, when compared with both the diabetic and metformin-treated diabetic groups. Moreover, co-administration of Zn and metformin significantly improved testicular histopathology, with a significant reduction in percent area of collagen fibers and nuclear factor kappa B (p65) immunoreactivity and a significant increase in seminiferous tubule diameter and connexin 43 immunoreactivity as compared with the diabetic and metformin-treated diabetic groups. In conclusion, the combination of Zn and metformin was an efficacious and safe alternative treatment, as it had superior antihyperglycemic efficacy and provided additional benefits over metformin alone in rats with type 2 diabetes.

UNLABELLED This study evaluates the effects produced by H2S donor; sodium hydrosulfide (NaHS), in a renal ischemia/reperfusion (IR) rat model and assesses the possible mediating role of nitric oxide (NO) in these H2S' effects. BACKGROUND For several centuries, hydrogen sulfide (H₂S) had been known to be a highly toxic agent. Recent studies, however, indicated that apart from NO and CO, H₂S is the third "gasotransmitter" involved in the regulation of various physiological functions. Nevertheless, its impact on renal IR injury remains unclear. METHODS Rats were randomly divided into three groups: sham control; renal IR; and renal IR+NaHS groups.NaHS (100 µmol/kg, ip) was administered 30 min prior to the induction of renal ischemia. RESULTS NaHS was found to attenuate significantly the IR-induced elevations in the serum levels of urea, creatinine and tumor necrosis factor α (TNF-α) as compared with IR group. NaHS also significantly compensated the deficits in the total antioxidant capacities (TAC) and lowered the elevated malondialdehyde (MDA) levels observed with renal IR in renal, hepatic, pulmonary, and cardiac tissues. Furthermore, NaHS pretreatment down-regulated the renal IR-induced over-expression of inducible nitric oxide synthase (iNOS) and up-regulated the IR-induced suppression of endothelial nitric oxide synthase (eNOS). The loss of normal architecture, hemorrhage, and inflammatory cells infiltration detected by histopathological examination of renal, hepatic, pulmonary, and cardiac tissues in IR rats were markedly ameliorated by pre-ischemic NaHS treatment. CONCLUSION NaHS protects against the effects of renal IR injury by acting primarily through a decrease in both pro-inflammatory cytokines and iNOS expression as well as through up-regulation of the eNOS pathway. Furthermore, H₂S has a powerful anti-oxidant and anti-apoptotic effects (Tab. 2, Fig. 6, Ref. 45).

BACKGROUND/PURPOSE: The effect of sofosbuvir and daclatasvir in treatment of genotype 4 Hepatitis C Virus (HCV) is not well documented. This study investigated the safety and efficacy of sofosbuvir plus daclatasvir with or without ribavirin in treatment of HCV genotype 4 patients. The impact of therapy on liver fibrosis as well as the role of IL18 polymorphism in therapeutic outcome was assessed. METHODS: One hundred HCV genotype 4 patients were categorized into 2 groups. The group 1 comprised treatment naïve patients, with total serum bilirubin ≤ 1.2 mg/10(−1) L, serum albumin ≥ 3.5 g/10(−1) L, INR ≤ 1.2, and platelet count ≥ 150 × 10(9)/L. This group was treated with sofosbuvir plus daclatasvir for 12 weeks. The group 2 included Peg-IFN-α-or sofosbuvir treatment experienced, or patients with at least 2 of the following findings: total serum bilirubin > 1.2 mg/10(−1) L, serum albumin 1.2, and platelet count

To investigate the effect of Ginsenoside-Rb1 (GRb1) on lithium (Li

Background: Metabolic syndrome (MetS) is a growing worldwide health problem. However, there is yet no effective therapy for MetS. The present work investigated the effect of liraglutide, a synthetic glucagon-like peptide-1 and vitamin E on fructose-induced MetS in rats. Summary: Liraglutide (0.3 mg/kg/day) and vitamin E (100 mg/kg/day) were administered either alone or in combination with high fructose-fed male rats for 6 weeks. Fructose-fed rats developed metabolic disorders assessed by visceral fat index, serum glucose, serum insulin, homeostasis model assessment-insulin resistance and serum lipids profile and hepatic disorders assessed by liver index, serum alanine aminotransferase and aspartate aminotransferase and steatohepatitis in histopathology. This study showed that liraglutide, vitamin E and their combination significantly ameliorated the fructose-induced metabolic and hepatic disorders. Key Messages: These results indicate a potential therapeutic benefit of liraglutide and vitamin E combination in prevention of MetS. Their protective effects might rely on their antioxidant effects as well as on the inhibition of tumor necrosis factor-α.

Acetaminophen (APAP) overdose is a common cause of acute liver failure, and beta-blockers are commonly used drugs in clinical practice. This study aimed to evaluate the effect of two different beta-blocker agents as nebivolol and atenolol against APAP-induced hepatotoxicity. Male Wistar rats were treated with APAP (2 g/kg/day, p.o.) to induce hepatotoxicity. Our results showed that nebivolol and atenolol reduced heart rate and blood pressure. Nebivolol (5 mg/kg/day, p.o.) for 14 days has a hepatoprotective effect shown by significant decrease in hepatic injury parameters (serum AST and ALT) with significant suppression of hepatic malondialdehyde (MDA) and nitric oxide (NO) which were elevated with APAP administration. Also, nebivolol increased reduced glutathione (GSH) which was reduced with APAP administration. Moreover, immunohistochemical examination revealed that nebivolol treatment markedly reduced inducible nitric oxide synthase (iNOS) expression, while expression of endothelial nitric oxide synthase (eNOS) was markedly enhanced, as compared to APAP group. The protective effects of nebivolol were also verified histopathologically. On the other hand, as compared to APAP group, oral administration of atenolol (50 mg/kg) increased hepatic injury parameters but did not change hepatic NO, MDA, and GSH. In conclusion, this study revealed that nebivolol not atenolol is protective against APAP-induced hepatotoxicity possibly, in part, through its antioxidant activity, inhibition of iNOS expression, and induction of eNOS expression.

Gentamicin, an aminoglycoside antibiotic, is used for the treatment of serious Gram-negative infections. However, its usefulness is limited by its nephrotoxicity. Sildenafil, a selective phosphodiesterase-5 inhibitor, was reported to prevent or decrease tissue injury. The aim of this study is to evaluate the potential protective effects of sildenafil on gentamicin-induced nephrotoxicity in rats. Male Wistar rats were injected with gentamicin (100 mg/kg/day, i.p.) for 6 days with and without sildenafil. Sildenafil administration resulted in nephroprotective effect in gentamicin-intoxicated rats as it significantly decreased serum creatinine and urea, urinary albumin, and renal malondialdehyde and nitrite/nitrate levels, with a concomitant increase in renal catalase and superoxide dismutase activities compared to gentamicin-treated rats. Moreover, immunohistochemical examination revealed that sildenafil treatment markedly reduced inducible nitric oxide synthase (iNOS) expression, while expression of endothelial nitric oxide synthase (eNOS) was markedly enhanced. The protective effects of sildenafil were verified histopathologically. In conclusion, sildenafil protects rats against gentamicin-induced nephrotoxicity possibly, in part, through its antioxidant activity, inhibition of iNOS expression, and induction of eNOS production.

Diabetic nephropathy results in end-stage renal disease. On the other hand, carvedilol has been reported to have various pharmacological properties. The aim of this study therefore is to evaluate the possible protective effect of carvedilol on streptozotocin-induced early diabetic nephropathy and various mechanisms underlie this effect in rats. Single i.p. injection of streptozotocin (65 mg/kg) was administered to induce early diabetic nephropathy in Wistar rats. Oral administration of carvedilol at a dose level of 1 and 10 mg/kg daily for 4 weeks resulted in nephroprotective effect as evident by significant decrease in serum creatinine level, urinary albumin/creatinine ratio, and kidney index as well as renal levels of malondialdehyde, nitric oxide, tumor necrosis factor-α, and cyclooxygenase-2 with a concurrent increase in creatinine clearance and renal reduced glutathione level compared to diabetic untreated rats. The protective effect of carvedilol was confirmed by renal histopathological examination. The electron microscopic examination indicated that carvedilol could effectively ameliorate glomerular basement membrane thickening and podocyte injury. In conclusion, carvedilol protects rats against streptozotocin-induced early diabetic nephropathy possibly, in part, through its antioxidant as well as anti-inflammatory activities, and ameliorating podocyte injury.

Methotrexate is an effective anticancer and immunosuppressive agent. However, nephrotoxicity is one of the complications of its use. On the other hand, curcumin, a naturally occurring polyphenolic compound, is reported to have antioxidant and anti-inflammatory properties. Those two properties are likely to prevent methotrexate-induced nephrotoxicity. The aim of this study is to evaluate the possible protective effect of curcumin against methotrexate-induced nephrotoxicity and delineate various mechanism(s) underlies this effect in rats. Nephrotoxicity was induced in Wistar rats by intraperitoneal administration of methotrexate (7 mg/kg/day) for three consecutive days. Curcumin administration in methotrexate-intoxicated rats resulted in nephroprotective effects as evidenced by the significant decrease in levels of serum creatinine and urea as well as renal malondialdehyde, nitric oxide, and tumor necrosis factor- α with a concurrent increase in renal glutathione peroxidase and superoxide dismutase activities compared to nephrotoxic untreated rats. Additionally, immunohistochemical analysis demonstrated that curcumin treatment markedly reduced cyclooxygenase-2 expression. Histopathological examination confirmed the protective effects of curcumin. In conclusion, curcumin protected rats from methotrexate nephrotoxicity, at least in part, through its antioxidant and anti-inflammatory activities.

Introduction and background Nosocomial pneumonia is the second most common nosocomial infection. It is usually bacterial in origin. Nosocomial pneumonia is responsible for 25% of infections in the ICU. Early-onset nosocomial pneumonia tends to carry a better prognosis than does late-onset nosocomial pneumonia. Patients and methods This study was planned to evaluate the role of the clinical pulmonary infection score (CPIS) and C-reactive protein (CRP) in detecting the efficacy of antibiotic therapy chosen for treatment of nosocomial Enterobacter pneumonia. In all, 200 patients admitted to the ICU who had evidence of pneumonia were included in the study. Patients were followed up by evaluating their serum CRP levels and CPIS during the first 8 days of admission. Results Enterobacter aerogenes represented 24% of nosocomial pneumonia cases in the study. An overall 70.8% of patients with E. aerogenes detected in culture and sensitivity were sensitive to both amikacin and levofloxacin. Those patients received only amikacin. Sixteen patients provided good response to amikacin. The remaining 18 patients showed poor response to amikacin therapy (proved by insignificant differences between CPIS and CRP on the first and fourth day of admission). In the case of these patients levofloxacin was added to antibiotic therapy and they were followed up for a further 4 days. The results demonstrated that 16 patients provided good response to amikacin and levofloxacin on the fifth and eighth days. Conclusion This study demonstrated that CPIS and serum CRP can be used as indicators of the efficacy of antibiotics in nosocomial pneumonia.

Aims: Male sub-fertility and infertility are major complications of diabetes mellitus. The non-selective β-blocker carvedilol has been reported to have favorable effects on some of the diabetic complications based on its antioxidant and anti-apoptotic effects. This study aims to evaluate the possible testicular protective effect of carvedilol in streptozotocin (STZ)-induced diabetic rat model and its possible mechanisms. Materials and Methods: Diabetes was induced by a single i.p. dose of 65 mg/kg of STZ. In parallel groups of diabetic rats, carvedilol in low and high doses (1 and 10 mg/kg/day orally) were administered for 4 weeks. Oxidative stress markers as reduced glutathione (GSH) and the product of lipid peroxidation; malondialdehyde (MDA) were evaluated in testicular homogenate. The level of expression of the apoptotic marker; caspase 3, was assessed using western blot, followed by densitometric analysis. Results: Induction of diabetes caused distortion of histological normal testicular structure, with decrease (P < 0.05) in GSH and increase (P < 0.05) in MDA, as well as induction of caspase 3 expression. Carvedilol in low or high doses reverted diabetes-induced histological damage, restored antioxidant activity and ameliorated caspase 3 expression. Conclusion: Carvedilol confers testicular protection against diabetes-induced damage through antioxidant and anti-apoptotic mechanisms.

SummaryA survey was made of academic difficulties among undergraduate students at Ain Shams University, Cairo, during the academic year 1979–1980. Almost 6% of students dropped out before graduating and a further 8% required substantial extra time to complete their course of study: these figures were almost identical for both sexes. Psychiatric disorders were diagnosed in 42% of male students with academic problems (compared with 9% among the academically successful), with neuroses accounting for nearly half of the cases and schizophrenia for a quarter. Serious psychiatric illness was nearly four times as frequent among 3rd-year students as among 1st-year students.

SummaryOne hundred and twenty-seven accidentally poisoned children from the emergency room of the Islamic Girls College, Cairo, were compared with an equal number of controls.The highest age incidence for both sexes in poisoned children was 36 months. Males outnumbered females at a ratio of 3:2. Behavioural problems such as hyperactivity, temper tantrums, aggression, stubbornness, nocturnal enuresis and impulsiveness occurred more often in poisoned children than in controls and more often in those (24 patients) referred with accidental poisoning on more than one occasion. The families of poisoned children differed significantly from the controls in their large size, low level of education, disturbed home atmosphere and the accessibility to the child of the poisonous substance.