Asbestos is known to induce oxidative stress in the lung. The consumption of butylated hydroxyanisole (BHA) in preserved food and soft drinks is increasing in the general population, which includes workers in asbestos factories. Because there is no information on the effect of co-exposure to chrysotile and BHA, the time-dependent effects of a single intratracheal dose of chrysotile (1 mg per mouse) and a single ip dose of BHA (350 mg/kg body weight) on various indices of oxidative stress such as lipid peroxidation, hydrogen peroxide generation, glutathione peroxidase (GPX), glutathione reductase (GR), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione (GSH) were followed for up to 14 days. Microsomal lipid peroxidation (as well as that induced by NADPH) was significantly enhanced by BHA in the chrysotile-exposed group. GPX and GR activities in the same group were gradually decreased by BHA. Non-significant modulation of catalase activity by BHA was also noted. BHA induces GSH to a significant extent in lungs exposed with chrysotile. An increase in the G6PDH activity was maximal (19%; P < 0.05) at day 3. The results clearly demonstrate that BHA enhances chrysotile-induced oxidative stress in the lung.

The involvement of reactive oxygen species (ROS) in the cytotoxicity of soot on rat alveolar macrophages has been postulated. A single intratracheal injection of soot (5 mg) in corn oil significantly induced the macrophage population, hydrogen peroxide (H2O2) generation, thiobarbituric acid (TBA)-reactive substances of lipid peroxidation, and the activities of extracellular acid phosphatase (AP) and lactate dehydrogenase (LDH) at 1, 4, 8, and 16 days of postinoculation. The activities of glutathione peroxidase (GPX) and catalase (CAT) were significantly inhibited at all the stages, while glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (G6PD) showed a different pattern. These results show that soot is cytotoxic to alveolar macrophages and suggest that ROS may play a primary role in the cytotoxic process.

The effects of a low protein diet on the body uptake and retention of cadmium, levels of essential trace elements, and cadmium-induced biochemical alterations in liver and kidneys of the rat were investigated. Low dietary protein disturbs cadmium induced alterations in carbohydrate metabolism, essential trace elements metabolism and offsets the hepatic and renal process of cadmium detoxification. Protein malnutrition enhances the susceptibility to cadmium intoxication.

The effect of vitamin B-complex on cadmium nephrotoxicity and hepatotoxicity was investigated in rats. The administration of Cd (3 mg per kg, s.c., three days) increased the urinary excretions of lactic dehydrogenase (LDH), glutamic oxalacetic transaminase (GOT), and total proteins, decreased renal activities LDH and GOT and increased concentration in kidney tissue of Cd, Cu, and Zn, Cadmium also increased serum BOT and glutamic pyruvic transaminase (GPT), decreased hepatic activities of GOT and GPT, and increased hepatic levels of Cd and Zn. The supplementation of vitamin B-complex (10 mg per kg, orally) simultaneously with Cd caused less marked biological alterations. Cadmium concentration in renal tissue was significantly less on the eighth day whereas the hepatic level of Cd was unaffected by vitamin supplementation. The protective effect of vitamin B-complex in Cd toxicity may be attributed to the interference by the constituents of vitamin B-complex in body absorption of Cd, possibly through forming readily excretable complexes. The results suggest that Cd toxicity can be reduced by vitamin B-complex supplementation.

The effect of nickel on cadmium nephro-toxicity and hepato-toxicity in rats was investigated. The administration of nickel (6 mg per kg, i.p., three days) or cadmium (6 mg per kg, i.m., once) significantly enhanced the urinary excretion of alkaline phosphatase (ALP), lactate dehydrogenase (LDH), glutamate oxaloacetate transaminase (GOT), amino acids, and proteins. In addition, it increased the activity of serum ALP, GOT, and glutamate pyruvate transaminase (GPT). These biochemical alterations in urine and serum were used as a measure of kidney and liver damage. Cadmium-induced enzymuria, proteinuria, amino aciduria and increase in the activity of serum enzymes were significantly less marked in animals pretreated with nickel than in controls. However, the accumulation of cadmium in kidneys and liver and its urinary excretion were unaffected by nickel pretreatment. The results suggest protection by nickel against cadmium nephro- and hepato-toxicity.

Influence of 2,3 dimercaptosuccinic acid, diethyldithiocarbamate and DL-penicillamine on the levels of essential metals in liver, kidney and serum was investigated. The hepatic zinc increased while renal copper decreased significantly upon treatment with these commonly used thiol metal chelators. On the other hand, hepatic copper decreased on treatment with DL-penicillamine. The renal zinc and serum copper and zinc remained practically unaffected on treatment with these metal chelators.

The role of selenium in protection against nephrotoxicity and hepatotoxicity of cadmium in rats was investigated. The administration of Cd (3 mg/kg, s.c.) for 3 days enhanced the urinary excretion of lactic dehydrogenase (LDH), glutamic oxaloacetic transaminase (GOT) and total proteins, decreased the renal activity of GOT and alkaline phosphatase (ALP) and increased the renal level of Cd, Cu and Zn. Cadmium also increased the serum GOT and glutamic pyruvic transaminase (GPT), decreased the hepatic activity of GOT and GPT and increased the hepatic level of Cd and Zn. The concomitantly administered Se (2 mg/kg, i.p.) initially reduced most of these Cd-induced alterations. The results show protection by Se against nephrotoxicity and hepatotoxicity of Cd on the 4th day of the commencement of Cd administration, but the signs of Cd intoxication were observed on the 8th day.