Ocular structure in vitamin A deficiency in the monkey

1. The role of vitamin A in the metabolism of cone cells of the retina was investigated, from the morphological angle, by studying their structure in induced deficiency of vitamin A in three monkeys. 2. Unequivocal signs of structural damage were observed in the cone and rod cells of the deficient animals, which also showed the classical signs of vitamin A deficiency in other organs. 3. In vitamin A deficiency, damage to the visual cell layer of the retina occurred in one monkey in the absence of corneal involvement. This finding suggests that chronic vitamin A deficiency in the community may lead to progressive damage to the visual cells in a much larger number of persons than the incidence figures for keratomalacia indicate. 4. Degeneration of pigment epithelium was present in retinal sections from all the deficient animals. The possible role of the pigment epithelium in the pathogenesis of the visual defect in vitamin A deficiency has been discussed. 5. Degenerative changes were noted in Descemet's endothelium. This damage may contribute to the degeneration of the corneal epithelium

Bhopal gas tragedy: scientific challenges and lessons for future

Some of the challenges of BGT were answered by two multi-disciplinary projects of the ICMR on Pathology and Toxicology and Pathophysiology. Unlike other chemical disasters, the aerosol inhaled by the Bhopal victims contained a mixture of MIC and its trimers and dimers, as well as aqueous and thermal decomposition products, including HCN. A coordinated GC-MS study of the blood and autopsy tissues and chemicals in the Tank residue confirmed their role. Autopsy studies revealed the pathological changes in the acute, sub-acute and chronic phases progressive changes of pulmonary edema and bronchiolitis, followed by chronic pulmonary fibrosis. Cerebral edema resulted in 'acute histotoxic anoxia'. Intensive experimental studies with the help of newer tools of molecular biology might throw more light on the underlying mechanisms and newer therapeutic approaches. The initial finding of cherry-red discoloration of lungs led to a suspicion of cyanide toxicity. Eventually, elevated blood and tissue cyanide levels confirmed the prompt therapeutic response to NaTS and accompanying increase of urinary NaSCN excretion. However, periodic clinical recurrences and relapses pointing towards 'chronic cyanide toxicity' remained enigmatic. Specific changes the 2-3 DPG levels and Blood Gases were explained on the basis of N-carbamoylation of end-terminal valine residues of Hb. Soon, several other end-terminal α-amino groups of tissue proteins were also found to be N-carbamoylated. Had the attempts at demonstrate S-carbamoylation of glutathione and other SH radicals of tissue enzymes like rhodanese succeeded, perhaps the underlying mechanism of chronic cyanide toxicity due to MIC might have been resolved. Based on the practical lessons learnt in Bhopal, an attempt will be made to present the salient pathological and toxicological findings, followed by a brief outline of the principles of planned laboratory management for alleviation of human suffering from future chemical disasters

Polyethylene Glycols as Embedding Media in Histochemical Work

This article does not have an abstract

Comparative toxicity of methyl isocyanate and its hydrolytic derivatives in rats. II. Pulmonary histopathology in the subacute and chronic phases

This paper describes the long-term (subacute and chronic) histopathological effects in the lungs of rats subjected to a single exposure to methyl isocyanate (MIC) by both the inhalation and subcutaneous (s.c.) routes as well as the role of methylamine (MA) and N,N'-dimethylurea (DMU), the hydrolytic derivatives of MIC in eliciting the observed changes. At the subacute phase, the intraalveolar and interstitial edema were prominent only in the inhalation group as against the more pronounced inflammatory response in the s.c. route. With the progress of time the evolution of lesions appeared to be similar, culminating in the development of significant interstitial pneumonitis and fibrosis. MA, one of the hydrolytic derivatives of MIC, also caused interstitial pneumonitis progressing to fibrosis, albeit to a lesser extent than MIC, indicating its contribution to the long-term pulmonary damage. The diffuse interstitial pulmonary fibrosis observed at 10 weeks after a single exposure to MIC by either route is of greater significance in the context of the occurrence of pulmonary fibrosis in the late autopsies of Bhopal gas victims and also clinical sequelae in some of the survivors

Comparative toxicity of methyl isocyanate and its hydrolytic derivatives in rats. I. Pulmonary histopathology in the acute phase

The present study describes the acute histopathological changes induced by methyl isocyanate (MIC) in the lungs of rats at 24 h after a single exposure to varied concentrations/doses of MIC by inhalation and subcutaneous (s.c.) routes and also delineates the effects due to the hydrolytic derivatives of MIC, viz., methylamine (MA) and N,N'-dimethyl urea (DMU). MIC, either inhaled or administered s.c., resulted in a wide range and extent of histopathological changes in the lungs, proportional to the exposure concentration/dose. The salient, effects of inhaled MIC are acute necrotizing bronchitis of the entire respiratory tract accompanied by varying degrees of confluent congestion, hyperemia and interstitial and intra-alveolar edema, while MIC administered s.c. led to prominent vascular endothelial damage, congestion and severe interstitial pneumonitis with apparently normal bronchial epithelium; and intra-alveolar edema only with the high dose. The only noteworthy lesion produced by MA and DMU (to some extent) was interstitial pneumonitis, suggesting their possible involvement in the subsequent inflammatory response of MIC. Except, for the endothelial changes, the overall spectrum of the histopathological lesions is quite comparable to those observed in the lungs of Bhopal victims during the acute phase

Caudal necrosis in suckling rats

The communication by Njaa et al. concerning the presence of 'ringtail' in newborn rats has prompted us to report similar observations in the colony maintained at these Laboratories. During the winter of 1954-55 signs of 'ringtail' were noticed in many suckling rats. Generally, these symptoms were seen in 8-day-old young rats, the first signs being a marked scaliness of the tail and reddening of the tail tip. In many cases the condition of the tail deteriorated, resulting in necrosis followed by its severance from the body. Microscopic examination of sections of the tails revealed in the early stages a marked hyperkeratosis and parakeratosis. There was dema (spongiosis) and hyperplasia of the prickle cell layer, resulting in acanthosis. In some of the specimens, the prickle cells at all levels contained large amounts of keratohyaline granules. The hair follicles were slightly dilated and were filled with keratinized invaginations of the cornified layers of the epidermis. The corium was dematous and often congested with blood. In the more advanced lesions, there was extensive eosinophilic necrosis of both the epidermis and the corium, accompanied by leucocytic infiltration. In general, these histological characters closely resemble those observed in the ring tails of rats born to mothers deprived of essential fatty acids

The effect of vitamin B12 on the toxicity of pyrimethamine (daraprim) in the monkey

This article does not have an abstract